6a.The nucleotide excision repair or NER is mechanism that has cap.pdf
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6a. The nucleotide excision repair or NER is mechanism that has capacity to repair the damaged nucleotide bases which are formed due to covalent interaction with large hydrocarbons and due to formation of pyrimidine dimers (T-T, T-C or CC), this mechanism of DNA repair is present in bacteria, yeast and mammalian cells. The damaged bases are first cut out within a string of nucleotides, and replaced with new DNA using undamaged strand as a complementary strand with the assistance of DNA polymerase and DNA ligase. In prokaryotes, the enzymes that perform NER because of UV damage or pyrimidine dimers are UvrABC excinuclease and the UvrD helicase. The genes responsible for their formation are named as uvrA, uvrB, uvrC and uvrD. The UvrABC complex first recognizes the damaged part of DNA, followed by cleavage on both sides of the demage, this damaged part is released by UvrD helicase that unwinds DNA using ATP molecules. The gap so created is filled by new DNA using DNA polymerase and the nick so created is later joined with main DNA on either by DNA ligase. In eukaryotes, it has been reported that Pol II (polB ) and Pol IV (dinB) does not affect them after UV irradiation or dimmer formation and only affects Pol V (umuC) Solution 6a. The nucleotide excision repair or NER is mechanism that has capacity to repair the damaged nucleotide bases which are formed due to covalent interaction with large hydrocarbons and due to formation of pyrimidine dimers (T-T, T-C or CC), this mechanism of DNA repair is present in bacteria, yeast and mammalian cells. The damaged bases are first cut out within a string of nucleotides, and replaced with new DNA using undamaged strand as a complementary strand with the assistance of DNA polymerase and DNA ligase. In prokaryotes, the enzymes that perform NER because of UV damage or pyrimidine dimers are UvrABC excinuclease and the UvrD helicase. The genes responsible for their formation are named as uvrA, uvrB, uvrC and uvrD. The UvrABC complex first recognizes the damaged part of DNA, followed by cleavage on both sides of the demage, this damaged part is released by UvrD helicase that unwinds DNA using ATP molecules. The gap so created is filled by new DNA using DNA polymerase and the nick so created is later joined with main DNA on either by DNA ligase. In eukaryotes, it has been reported that Pol II (polB ) and Pol IV (dinB) does not affect them after UV irradiation or dimmer formation and only affects Pol V (umuC).
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Dna repair mechanisms
DNA repair mechanisms in prokaryotes involve direct repair, excision repair, and mismatch repair. Direct repair converts damaged nucleotides directly back to their original structure using enzymes like photolyase. Excision repair removes damaged sections of DNA through base excision repair which removes single damaged bases using glycosylases and AP endonucleases, or nucleotide excision repair which removes short oligonucleotides. Mismatch repair recognizes and fixes errors made during DNA replication by distinguishing the parental DNA strands and excising the newly synthesized strand containing mistakes.
DNA REPAIR MECHANSIMS (2).pptx
DNA repair system lecture that were prepered by Ph.D. students Mohammed Mohsen and Aliaa Hashim at microbiology department / college of medicine / babylon university.
DNA repair by k sahu
Introduction
Enzyme involve of DNA repair
Types of DNA repair
direct DNA repair
excision repair system
mismatch repair system
Conclusion
Reference
DNA polymerase –a class of enzyme to all synthesize 5’ to 3’ direction of nucleotides.
DNA polymerase I – a class of enzyme 1st isolated by Escherichia coli, and function is removes of RNA primers ,during DNA replication.
Helicase- any of a group of enzyme that unwind the two strand of DNA to facilitate DNA replication.
Exonuclease – an enzyme capable of cutting phosphodiester bonds between nucleotides located at an end of a DNA strand .
Endonuclease – an enzyme capable of cleaving phosphodiester bonds between nucleotide located internally in a DNA strand .
DNA ligase – a enzyme that fill the gap of nucleotides.
DNA repair
The document discusses various types of DNA damage including deamination, depurination, UV light-induced T-T and T-C dimers, alkylation, oxidative damage, replication errors, and double-strand breaks. It then summarizes different DNA repair pathways such as base excision repair, nucleotide excision repair, mismatch repair, direct repair, recombination repair, and non-homologous end-joining. The SOS response in bacteria is also summarized as activating error-prone repair when normal repair pathways are overwhelmed.
DNA as the Genetic material,DNA damage and Repair Mechanism
1. Experiments in the 1940s-1950s provided evidence that DNA, not protein, is the genetic material. This included Avery, MacLeod and McCarty's experiment showing only DNA could transform bacteria.
2. Further evidence came from Hershey and Chase's experiment labelling bacterial virus DNA and protein differently, finding that DNA entered host bacteria cells while protein did not.
3. DNA can be damaged by various agents like radiation, chemicals, and oxidation. Cells have multiple DNA repair mechanisms like base-excision repair and nucleotide-excision repair to repair damages and prevent mutations.
Excision repair in dna
This document summarizes different types of DNA repair mechanisms including base excision repair, nucleotide excision repair, and their mechanisms in E. coli and humans. It also discusses short patch and long patch base excision repair, and conditions like xeroderma pigmentosum that arise from defects in nucleotide excision repair.
Dna repair mechanism
1. DNA repair mechanisms include direct reversal and excision repair. Excision repair involves removing the damaged nucleotide using the undamaged strand as a template for replacement.
2. The two main excision repair systems are base excision repair and nucleotide excision repair. Base excision repair involves removing the damaged base using glycosylases and nucleotide excision repair removes a short strand containing the lesion.
3. Defects in nucleotide excision repair can lead to conditions like xeroderma pigmentosum where ultraviolet radiation damage cannot be repaired, increasing skin cancer risks.
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Dna repair mechanisms
DNA repair mechanisms in prokaryotes involve direct repair, excision repair, and mismatch repair. Direct repair converts damaged nucleotides directly back to their original structure using enzymes like photolyase. Excision repair removes damaged sections of DNA through base excision repair which removes single damaged bases using glycosylases and AP endonucleases, or nucleotide excision repair which removes short oligonucleotides. Mismatch repair recognizes and fixes errors made during DNA replication by distinguishing the parental DNA strands and excising the newly synthesized strand containing mistakes.
DNA REPAIR MECHANSIMS (2).pptx
DNA repair system lecture that were prepered by Ph.D. students Mohammed Mohsen and Aliaa Hashim at microbiology department / college of medicine / babylon university.
DNA repair by k sahu
Introduction
Enzyme involve of DNA repair
Types of DNA repair
direct DNA repair
excision repair system
mismatch repair system
Conclusion
Reference
DNA polymerase –a class of enzyme to all synthesize 5’ to 3’ direction of nucleotides.
DNA polymerase I – a class of enzyme 1st isolated by Escherichia coli, and function is removes of RNA primers ,during DNA replication.
Helicase- any of a group of enzyme that unwind the two strand of DNA to facilitate DNA replication.
Exonuclease – an enzyme capable of cutting phosphodiester bonds between nucleotides located at an end of a DNA strand .
Endonuclease – an enzyme capable of cleaving phosphodiester bonds between nucleotide located internally in a DNA strand .
DNA ligase – a enzyme that fill the gap of nucleotides.
DNA repair
The document discusses various types of DNA damage including deamination, depurination, UV light-induced T-T and T-C dimers, alkylation, oxidative damage, replication errors, and double-strand breaks. It then summarizes different DNA repair pathways such as base excision repair, nucleotide excision repair, mismatch repair, direct repair, recombination repair, and non-homologous end-joining. The SOS response in bacteria is also summarized as activating error-prone repair when normal repair pathways are overwhelmed.
DNA as the Genetic material,DNA damage and Repair Mechanism
1. Experiments in the 1940s-1950s provided evidence that DNA, not protein, is the genetic material. This included Avery, MacLeod and McCarty's experiment showing only DNA could transform bacteria.
2. Further evidence came from Hershey and Chase's experiment labelling bacterial virus DNA and protein differently, finding that DNA entered host bacteria cells while protein did not.
3. DNA can be damaged by various agents like radiation, chemicals, and oxidation. Cells have multiple DNA repair mechanisms like base-excision repair and nucleotide-excision repair to repair damages and prevent mutations.
Excision repair in dna
This document summarizes different types of DNA repair mechanisms including base excision repair, nucleotide excision repair, and their mechanisms in E. coli and humans. It also discusses short patch and long patch base excision repair, and conditions like xeroderma pigmentosum that arise from defects in nucleotide excision repair.
Dna repair mechanism
1. DNA repair mechanisms include direct reversal and excision repair. Excision repair involves removing the damaged nucleotide using the undamaged strand as a template for replacement.
2. The two main excision repair systems are base excision repair and nucleotide excision repair. Base excision repair involves removing the damaged base using glycosylases and nucleotide excision repair removes a short strand containing the lesion.
3. Defects in nucleotide excision repair can lead to conditions like xeroderma pigmentosum where ultraviolet radiation damage cannot be repaired, increasing skin cancer risks.
DNA REPAIR MECHANISMS.pptx
DNA repair mechanisms identify and correct damage to DNA. There are two main types of DNA damage: endogenous damage caused by metabolic byproducts, and exogenous damage caused by external factors like radiation or toxins. The main DNA repair pathways are direct reversal, base excision repair, nucleotide excision repair, mismatch repair, nonhomologous end joining, and homologous recombination. These pathways utilize various enzymes to recognize damage, cut and remove damaged sections of DNA, and use undamaged DNA as a template for repair synthesis to restore the proper DNA sequence. Defects in certain DNA repair pathways can cause human diseases like xeroderma pigmentosum or Cockayne syndrome.
21 gouiaa
This document summarizes the mechanisms of DNA repair. It discusses various types of DNA damage including tautomerization, deamination, oxidation, alkylation, and pyrimidine dimers. The main DNA repair mechanisms are damage reversal, damage removal, and damage tolerance. Damage reversal includes photoreactivation and direct repair enzymes. Damage removal consists of base excision repair, nucleotide excision repair, and mismatch repair. Damage tolerance uses error-prone repair or double-strand break repair. Accumulation of unrepaired DNA damage over time contributes to aging.
DNA damage and repair systems
DNA is constantly damaged by environmental and cellular factors, causing over 100,000 lesions per day. To prevent disease, cells have multiple repair pathways including base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. Base excision repair fixes small base damages through removal and replacement. Nucleotide excision repair removes larger helix-distorting lesions by cleaving and synthesizing new DNA. Mismatch repair recognizes and fixes errors made during DNA replication. Double-strand break repair uses either non-homologous end joining or homologous recombination to reconnect broken DNA ends. Defects in these pathways compromise genomic integrity and can cause cancer or other genetic disorders.
Dna damage. lgis
The document discusses DNA damage and repair mechanisms in human cells. It begins by explaining how errors can occur during DNA replication and how environmental agents like chemicals and radiation can damage DNA. It then describes different types of DNA damage and several pathways cells use to repair damaged DNA, including direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. It provides details on these repair mechanisms and how they work to recognize and remove damaged sections of DNA before replacing them. The document concludes by discussing some genetic diseases associated with defects in DNA repair systems, like xeroderma pigmentosum, progeria, and Werner syndrome.
The DNA Damage Repair Response
Each day the genome is subjected to thousands of DNA damaging events from diverse sources which can have potentially deleterious consequences. In order to maintain genome integrity eukaryotic cells have evolved a highly complex and multifaceted response network called the DNA damage response, or ?DDR?....
The DNA Damage Repair Response
Each day the genome is subjected to thousands of DNA damaging events from diverse sources which can have potentially deleterious consequences. In order to maintain genome integrity eukaryotic cells have evolved a highly complex and multifaceted response network called the DNA damage response, or ?DDR?
The DNA Damage Repair Response
Each day the genome is subjected to thousands of DNA damaging events from diverse sources which can have potentially deleterious consequences. In order to maintain genome integrity eukaryotic cells have evolved a highly complex and multifaceted response network called the DNA damage response
The DNA Damage Repair Response
The document summarizes various pathways that cells use to repair DNA damage, including direct repair, base excision repair, mismatch repair, nucleotide excision repair, and non-homologous end joining. It describes how each pathway is initiated, the key proteins involved, and how the damaged DNA is repaired. It highlights the complexity of the DNA damage response and importance of accurate repair to prevent mutations that could lead to cancer.
Each day the genome is subjected to thousands of DNA damaging events from div...
Each day the genome is subjected to thousands of DNA damaging events from diverse sources which can have potentially deleterious consequences. In order to maintain genome integrity eukaryotic cells have evolved a highly complex and multifaceted response network called the DNA damage response, or ?DDR?..
DNA repair system_mechanism
DNA repair systems are critical for correcting damage to DNA that occurs naturally. There are multiple DNA repair mechanisms that have been discovered, including direct reversal of damage, mismatch repair, recombinational repair, and excision repair. Excision repair involves removing damaged sections of DNA. It is a conserved process in prokaryotes and eukaryotes that utilizes DNA glycosylases to recognize and remove damaged bases, AP endonucleases to excise areas around the damaged bases, DNA polymerase to fill in the gaps, and DNA ligase to seal the gaps.
DNA damages and repair
An overview of DNA damages and repair mechanism and the source of presentation is greatly acknowledged
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This document discusses DNA damage and repair mechanisms. It begins by introducing DNA damage and its sources, including endogenous sources like reactive oxygen species and exogenous sources like radiation. It then describes different types of DNA damage such as single base alterations, double base alterations, chain breaks, and cross-linkages. The document proceeds to explain four main DNA repair pathways: photoreactivation, base excision repair, nucleotide excision repair, and mismatch repair. Each repair pathway involves specific enzymes to identify and remove damaged DNA and allow for new DNA synthesis. In summary, the document provides an overview of DNA damage sources and types as well as the key repair mechanisms cells use to correct DNA damage.
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DNA repair is a collection of processes cells use to identify and correct damage to DNA molecules. Without repair, a cell cannot maintain its essential functions and DNA damage may lead to mutations or cell death. The main types of DNA repair are direct repair, nucleotide excision repair, base excision repair, and SOS repair. Defects in DNA repair can cause diseases like xeroderma pigmentosum where individuals are sensitive to sunlight and prone to skin cancer.
Dna damage and repair
DNA in cells can become damaged through radiation, chemicals, and errors during replication. There are several pathways cells use to repair DNA damage, including direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Double strand breaks can be repaired through direct joining of broken ends or homologous recombination using the sister chromatid as a template. Failure to properly repair DNA damage can lead to mutations and genetic disorders.
Lecture DNA repair - Part-1_slideshare.pdf
This document discusses DNA repair mechanisms, specifically nucleotide excision repair. It provides details on:
1) Nucleotide excision repair is a mechanism to repair DNA damage such as thymine dimers caused by UV light. It involves the uvrA, uvrB, uvrC, and uvrD genes which encode proteins that recognize distortions in DNA structure and cut out the damaged region for replacement.
2) If nucleotide excision repair fails, it can result in genetic disorders like xeroderma pigmentosum which increases skin cancer risk, or Cockayne syndrome which involves neurological issues.
Dna repair
1. DNA repair is a collection of processes by which cells identify and correct damage to DNA molecules to maintain the integrity of the genome.
2. There are several pathways of DNA repair including base excision repair, nucleotide excision repair, mismatch repair, non-homologous end joining, and homologous recombination.
3. Defects in DNA repair pathways can lead to increased mutations, cancer, and cell death if damage is left unrepaired.
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DNA Damage Repair mechanisms.pdf
(I) DNA can be damaged by radiation, chemicals, and other environmental factors which cells have developed mechanisms to repair. (II) There are direct repair systems like photoreactivation and base excision repair that remove damaged bases. (III) Nucleotide excision repair and mismatch repair pathways cut out the damaged DNA section and resynthesize the correct sequence. (IV) Double strand breaks are repaired by nonhomologous end joining or homologous recombination.
DNA damage and Repair mechanism and types
DNA is constantly damaged by radiation, chemicals, and other agents. There are multiple pathways for repairing DNA damage, including direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Base excision repair removes individual damaged bases. Nucleotide excision repair removes short fragments of 24-32 bases to repair more substantial damage like thymine dimers. Mismatch repair recognizes and fixes incorrect incorporations during DNA replication. Together, these pathways help maintain the integrity of DNA.
NER pathway
Nucleotide excision repair (NER) is a pathway that repairs a broad class of helix-distorting lesions in DNA that disrupt transcription and replication. It involves recognizing the damaged site, unwinding the DNA helix, making dual incisions on both sides of the damage, excising the damaged fragment, and resynthesizing the replacement DNA. NER is a complex process involving at least 28 genes and is important for repairing UV-induced damage and protecting against sunlight-induced DNA damage and cancer. Defects in NER genes can cause diseases like xeroderma pigmentosum, trichothiodystrophy, and Cockayne syndrome.
The Arrhenius Theory of acids and bases The theo.pdf
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produce hydrogen ions in solution. Bases are substances which produce hydroxide ions in
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Solution
The Arrhenius Theory of acids and bases The theory Acids are substances which
produce hydrogen ions in solution. Bases are substances which produce hydroxide ions in
solution. HBr------>H+ + Br- since HBr is capable of producing H+ it is an acid.
oxygen in air (O2) reacts with H2 when it burns .pdf
oxygen in air (O2) reacts with H2 when it burns H2 + 2O2 = 2H2O
Solution
oxygen in air (O2) reacts with H2 when it burns H2 + 2O2 = 2H2O.
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DNA REPAIR MECHANISMS.pptx
DNA repair mechanisms identify and correct damage to DNA. There are two main types of DNA damage: endogenous damage caused by metabolic byproducts, and exogenous damage caused by external factors like radiation or toxins. The main DNA repair pathways are direct reversal, base excision repair, nucleotide excision repair, mismatch repair, nonhomologous end joining, and homologous recombination. These pathways utilize various enzymes to recognize damage, cut and remove damaged sections of DNA, and use undamaged DNA as a template for repair synthesis to restore the proper DNA sequence. Defects in certain DNA repair pathways can cause human diseases like xeroderma pigmentosum or Cockayne syndrome.
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This document summarizes the mechanisms of DNA repair. It discusses various types of DNA damage including tautomerization, deamination, oxidation, alkylation, and pyrimidine dimers. The main DNA repair mechanisms are damage reversal, damage removal, and damage tolerance. Damage reversal includes photoreactivation and direct repair enzymes. Damage removal consists of base excision repair, nucleotide excision repair, and mismatch repair. Damage tolerance uses error-prone repair or double-strand break repair. Accumulation of unrepaired DNA damage over time contributes to aging.
DNA damage and repair systems
DNA is constantly damaged by environmental and cellular factors, causing over 100,000 lesions per day. To prevent disease, cells have multiple repair pathways including base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. Base excision repair fixes small base damages through removal and replacement. Nucleotide excision repair removes larger helix-distorting lesions by cleaving and synthesizing new DNA. Mismatch repair recognizes and fixes errors made during DNA replication. Double-strand break repair uses either non-homologous end joining or homologous recombination to reconnect broken DNA ends. Defects in these pathways compromise genomic integrity and can cause cancer or other genetic disorders.
Dna damage. lgis
The document discusses DNA damage and repair mechanisms in human cells. It begins by explaining how errors can occur during DNA replication and how environmental agents like chemicals and radiation can damage DNA. It then describes different types of DNA damage and several pathways cells use to repair damaged DNA, including direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. It provides details on these repair mechanisms and how they work to recognize and remove damaged sections of DNA before replacing them. The document concludes by discussing some genetic diseases associated with defects in DNA repair systems, like xeroderma pigmentosum, progeria, and Werner syndrome.
The DNA Damage Repair Response
Each day the genome is subjected to thousands of DNA damaging events from diverse sources which can have potentially deleterious consequences. In order to maintain genome integrity eukaryotic cells have evolved a highly complex and multifaceted response network called the DNA damage response, or ?DDR?....
The DNA Damage Repair Response
Each day the genome is subjected to thousands of DNA damaging events from diverse sources which can have potentially deleterious consequences. In order to maintain genome integrity eukaryotic cells have evolved a highly complex and multifaceted response network called the DNA damage response, or ?DDR?
The DNA Damage Repair Response
Each day the genome is subjected to thousands of DNA damaging events from diverse sources which can have potentially deleterious consequences. In order to maintain genome integrity eukaryotic cells have evolved a highly complex and multifaceted response network called the DNA damage response
The DNA Damage Repair Response
The document summarizes various pathways that cells use to repair DNA damage, including direct repair, base excision repair, mismatch repair, nucleotide excision repair, and non-homologous end joining. It describes how each pathway is initiated, the key proteins involved, and how the damaged DNA is repaired. It highlights the complexity of the DNA damage response and importance of accurate repair to prevent mutations that could lead to cancer.
Each day the genome is subjected to thousands of DNA damaging events from div...
Each day the genome is subjected to thousands of DNA damaging events from diverse sources which can have potentially deleterious consequences. In order to maintain genome integrity eukaryotic cells have evolved a highly complex and multifaceted response network called the DNA damage response, or ?DDR?..
DNA repair system_mechanism
DNA repair systems are critical for correcting damage to DNA that occurs naturally. There are multiple DNA repair mechanisms that have been discovered, including direct reversal of damage, mismatch repair, recombinational repair, and excision repair. Excision repair involves removing damaged sections of DNA. It is a conserved process in prokaryotes and eukaryotes that utilizes DNA glycosylases to recognize and remove damaged bases, AP endonucleases to excise areas around the damaged bases, DNA polymerase to fill in the gaps, and DNA ligase to seal the gaps.
DNA damages and repair
An overview of DNA damages and repair mechanism and the source of presentation is greatly acknowledged
Manisha 4th ppt
This document discusses DNA damage and repair mechanisms. It begins by introducing DNA damage and its sources, including endogenous sources like reactive oxygen species and exogenous sources like radiation. It then describes different types of DNA damage such as single base alterations, double base alterations, chain breaks, and cross-linkages. The document proceeds to explain four main DNA repair pathways: photoreactivation, base excision repair, nucleotide excision repair, and mismatch repair. Each repair pathway involves specific enzymes to identify and remove damaged DNA and allow for new DNA synthesis. In summary, the document provides an overview of DNA damage sources and types as well as the key repair mechanisms cells use to correct DNA damage.
DNA_repair 2.pptx
DNA repair is a collection of processes cells use to identify and correct damage to DNA molecules. Without repair, a cell cannot maintain its essential functions and DNA damage may lead to mutations or cell death. The main types of DNA repair are direct repair, nucleotide excision repair, base excision repair, and SOS repair. Defects in DNA repair can cause diseases like xeroderma pigmentosum where individuals are sensitive to sunlight and prone to skin cancer.
Dna damage and repair
DNA in cells can become damaged through radiation, chemicals, and errors during replication. There are several pathways cells use to repair DNA damage, including direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Double strand breaks can be repaired through direct joining of broken ends or homologous recombination using the sister chromatid as a template. Failure to properly repair DNA damage can lead to mutations and genetic disorders.
Lecture DNA repair - Part-1_slideshare.pdf
This document discusses DNA repair mechanisms, specifically nucleotide excision repair. It provides details on:
1) Nucleotide excision repair is a mechanism to repair DNA damage such as thymine dimers caused by UV light. It involves the uvrA, uvrB, uvrC, and uvrD genes which encode proteins that recognize distortions in DNA structure and cut out the damaged region for replacement.
2) If nucleotide excision repair fails, it can result in genetic disorders like xeroderma pigmentosum which increases skin cancer risk, or Cockayne syndrome which involves neurological issues.
Dna repair
1. DNA repair is a collection of processes by which cells identify and correct damage to DNA molecules to maintain the integrity of the genome.
2. There are several pathways of DNA repair including base excision repair, nucleotide excision repair, mismatch repair, non-homologous end joining, and homologous recombination.
3. Defects in DNA repair pathways can lead to increased mutations, cancer, and cell death if damage is left unrepaired.
2_5332278739243900645.ppt
We report a previously unrecognized mechanism whereby IL-36 promotes innate antiviral immunity in mouse and human models of herpes simplex virus ...
DNA Damage Repair mechanisms.pdf
(I) DNA can be damaged by radiation, chemicals, and other environmental factors which cells have developed mechanisms to repair. (II) There are direct repair systems like photoreactivation and base excision repair that remove damaged bases. (III) Nucleotide excision repair and mismatch repair pathways cut out the damaged DNA section and resynthesize the correct sequence. (IV) Double strand breaks are repaired by nonhomologous end joining or homologous recombination.
DNA damage and Repair mechanism and types
DNA is constantly damaged by radiation, chemicals, and other agents. There are multiple pathways for repairing DNA damage, including direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Base excision repair removes individual damaged bases. Nucleotide excision repair removes short fragments of 24-32 bases to repair more substantial damage like thymine dimers. Mismatch repair recognizes and fixes incorrect incorporations during DNA replication. Together, these pathways help maintain the integrity of DNA.
NER pathway
Nucleotide excision repair (NER) is a pathway that repairs a broad class of helix-distorting lesions in DNA that disrupt transcription and replication. It involves recognizing the damaged site, unwinding the DNA helix, making dual incisions on both sides of the damage, excising the damaged fragment, and resynthesizing the replacement DNA. NER is a complex process involving at least 28 genes and is important for repairing UV-induced damage and protecting against sunlight-induced DNA damage and cancer. Defects in NER genes can cause diseases like xeroderma pigmentosum, trichothiodystrophy, and Cockayne syndrome.
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Each day the genome is subjected to thousands of DNA damaging events from div...
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return coodX3;
}
public void setCoodX3(double coodX3) {
this.coodX3 = coodX3;
}
public double getCoodY3() {
return coodY3;
}
public void setCoodY3(double coodY3) {
this.coodY3 = coodY3;
}
//This method will calculate the distance between the point
public double distance(double x1,double y1,double x2,double y2)
{
return Math.sqrt(Math.pow((x2-x1),2)+Math.pow((y2-y1),2));
}
//This method will calculate the angle between the two points
public double angleOfPoints(double x1,double y1,double x2,double y2)
{
double xDiff=x2-x1;
double yDiff=y2-y1;
double angle=Math.atan2(yDiff, xDiff)*(180/Math.PI);
return angle;
}
//This method will calculate the area of the triangle
public double getArea()
{
double lengthA=distance(getCoodX1(),getCoodY1(), getCoodX2(), getCoodY2());
double lengthB=distance(getCoodX2(),getCoodY2(), getCoodX3(), getCoodY3());
double lengthC=distance(getCoodX3(),getCoodY3(), getCoodX1(), getCoodY1());
double S=(lengthA+lengthB+lengthC)/2;
//Calculating the area
double area=Math.sqrt(S*(S-lengthA)*(S-lengthB)*(S-lengthC));
return area;
}
//This method will calculate the Perimeter of the triangle
public double getPerimeter()
{
double lengthA=distance(getCoodX1(),getCoodY1(), getCoodX2(), getCoodY2());
double lengthB=distance(getCoodX2(),getCoodY2(), getCoodX3(), getCoodY3());
double lengthC=distance(getCoodX3(),getCoodY3(), getCoodX1(), getCoodY1());
//Calculating the perimter
double S=(lengthA+lengthB+lengthC);
return S;
}
//Displaying the triangle is isosceles triangle or not
public void Isosceles()
{
double lengthA=distance(getCoodX1(),getCoodY1(), getCoodX2(), getCoodY2());
double lengthB=distance(getCoodX2(),getCoodY2(), getCoodX3(), getCoodY3());
double lengthC=distance(getCoodX3(),getCoodY3(), getCoodX1(), getCoodY1());
if((lengthA==lengthB) || (lengthB==lengthC) || (lengthC==lengthA) )
{
System.out.println(\":: The Triangle is Isosceles ::\");
}
else
System.out.println(\":: The Triangle is Not Isosceles ::\");
}
//.
There is some data missing in the problem.The composition of the m.pdf
There is some data missing in the problem.
The composition of the mixture and the reaction taking place need to be mentioned. The total
experiment might help
Moles of CaC2O4. H2O = mass/ molar mass
= 1.075 g / 146.11 g/mol
= 0.0074 moles
Solution
There is some data missing in the problem.
The composition of the mixture and the reaction taking place need to be mentioned. The total
experiment might help
Moles of CaC2O4. H2O = mass/ molar mass
= 1.075 g / 146.11 g/mol
= 0.0074 moles.
at beginning flask has only NaOH pH = 14 + log [N.pdf
at beginning flask has only NaOH pH = 14 + log [NaOH] =14+log[1] = 14
{[NaOH]= conc. of naoh in Mole/liter = 1 (given)}
Solution
at beginning flask has only NaOH pH = 14 + log [NaOH] =14+log[1] = 14
{[NaOH]= conc. of naoh in Mole/liter = 1 (given)}.
take log on both sides1n lna = ln las a--0.pdf
take log on both sides
1/n lna = ln l
as a--0
l= e^ 0 =1
Solution
take log on both sides
1/n lna = ln l
as a--0
l= e^ 0 =1.
Tested on Eclipse and both class should be in same packageimport.pdf
//Tested on Eclipse and both class should be in same package
import java.util.Scanner;
public class P3 {
/*isInteger method implementation
* @param String type
* while parsing if it throw exception then it is not integer
* else it is integer*/
public static Boolean isDouble(String token){
try {
Double.parseDouble(token);
} catch(NumberFormatException e) {
System.out.println(\"Invalid Operand\");
return false;
} catch(NullPointerException e) {
System.out.println(\"Invalid Operand\");
return false;
}
// only got here if we didn\'t return false
return true;
}
public static String evaluate(String expression) {
// Print expression
System.out.print(expression);
// Declare variables for operands, operator, result, and return value
double operand1=0,operand2 = 0,result=0;
char operator;
Boolean flag=Boolean.FALSE;//for if operators were not listed
String returnString = \"\";
String token[]=new String[expression.length()];//for storing all token from expression
// Create Scanner object to parse expression
// create a new scanner with the specified String Object
int i=0;
Scanner scanner = new Scanner(expression);
while(scanner.hasNext()){
token[i]=scanner.next();
i++;
}
scanner.close();
// Compute a numerical result for the expression
if(isDouble(token[0])){
operand1=Double.parseDouble(token[0]);
}
if(isDouble(token[2])){
operand2=Double.parseDouble(token[2]);
}
operator=token[1].charAt(0);
if(operand1!=0&&operand2!=0){
switch(operator){
case \'+\':
result=operand1+operand2;
break;
case \'-\':
result=operand1-operand2;
break;
case \'*\':
result=operand1*operand2;
break;
case \'/\':
result=operand1/operand2;
break;
case \'%\':
result=operand1%operand2;
break;
case \'^\':
result=Math.pow(operand1, operand2);
break;
default:
System.out.println(\"Invalid Operator\");
flag=Boolean.TRUE;
break;
}
// Convert numerical result to string
returnString=Double.toString(result);
if(flag){
return null;
}
// Return result
return returnString;
}else{
return null;
}
}
}
/*********Calculator class***************/
import java.util.Scanner;
/*Calculator class start*/
public class Calculator {
public static void main(String args[]){
/*Variable declaration*/
String expression;
/*Scanner object for input*/
Scanner input=new Scanner(System.in);
/*Prompt for expression*/
System.out.println(\"Please Enter expression\");
expression=input.nextLine();
input.close();
/*Calling Evaluate method*/
String result=P3.evaluate(expression);
/*Printing result if it is not null*/
if(result!=null) {
System.out.println(result);
}
}
}
/***************output************/
Please Enter expression
11.22 + 3.456 =
11.22 + 3.456 =14.676
Please Enter expression
5.555 - 32.14 =
5.555 - 32.14 =-26.585
Please Enter expression
25634.8 * .32 =
25634.8 * .32 = 8203.136
Please Enter expression
5 ^ 4 =
5 ^ 4 =625.0
Please Enter expression
Whatever + 2 =
Whatever + 2 =Invalid Operand
Please Enter expression
4.0 - 1.2.3 =
4.0 - 1.2.3 =Invalid Operand
Please Enter expression
1.234 $ 0.5 =
1.234 $ 0.5 =Invalid Ope.
Solution A person in perfect health has a utility score of 1.0U.pdf
Solution
:
A person in perfect health has a utility score of 1.0
Utility of a person having some cognitive problems and some social problems = 1 - 0.35 - 0.29
Utility of a person having some cognitive problems and some social problems = 0.36.
Resurgent infection is suggesting that it is viral infection by meas.pdf
Resurgent infection is suggesting that it is viral infection by measles virus S. In this disease
patients have fever above 101 °F with diarrhea.
Possible reason would be the vaccination in 1963 didn’t work properly and some of the patients
got immuned for the virus. The remaining patients latterly increased infection by transmitting
means.
Herd immunity is termed when a large population or a community get immuned to an infection.
In this case 18, 193 cases of 1989 got herd immunity because the next year number increased
largely.
In US the vaccine, Measles, mumps, and rubella (MMR) vaccine, is administered in between 12
months to 4 years age.
Solution
Resurgent infection is suggesting that it is viral infection by measles virus S. In this disease
patients have fever above 101 °F with diarrhea.
Possible reason would be the vaccination in 1963 didn’t work properly and some of the patients
got immuned for the virus. The remaining patients latterly increased infection by transmitting
means.
Herd immunity is termed when a large population or a community get immuned to an infection.
In this case 18, 193 cases of 1989 got herd immunity because the next year number increased
largely.
In US the vaccine, Measles, mumps, and rubella (MMR) vaccine, is administered in between 12
months to 4 years age..
There are only two functional groups in the molec.pdf
There are only two functional groups in the molecule: -OH (alcohol) -COO- (ester)
Any other functional group is not found in the molecule
Solution
There are only two functional groups in the molecule: -OH (alcohol) -COO- (ester)
Any other functional group is not found in the molecule.
PsychoanalysisPsychoanalysis was founded by Sigmund Freud (1856-19.pdf
Psychoanalysis
Psychoanalysis was founded by Sigmund Freud (1856-1939). Freud believed that people could
be cured by making conscious their unconscious thoughts and motivations, thus gaining insight.
The aim of psychoanalysis therapy is to release repressed emotions and experiences, i.e. make
the unconscious conscious.
The basic tenets of psychoanalysis include:
Psychoanalysis designates concomitantly three things:
Confrontation
This is a practice often done prior to an intervention where the patient is encouraged to attend to
experiences that they have been avoiding.
Countertransference
This refers to the analyst’s feelings and attitudes towards the patient: his/her reaction to the
patient’s transference, how his/her own experiences impact his/her understanding of the patient,
and the analyst’s emotional responses to the patient.
Defense Mechanisms
Defense mechanisms are used by the ego as a way to deal with conflict of problems in life.
Operating at an unconscious level, defense mechanisms help to reduce negative feelings (e.g.
anxiety and guilt). Common defense mechanisms include repression, denial, and projection.
Dream
It is a mental event that consists of hallucinations involving imagery and emotions. Dreams
occur during the rapid-eye movement (REM) stage during sleep. According to Freud, current
concerns and unconscious childhood wishes are present during the day and require gratification
and it is dreams that allow us to respond to this demands while continuing to sleep (e.g., a person
who is thirsty dreams about drinking water which allows him to continue sleeping rather than
having to wake up and satisfy his thirst)
Ego
Sigmund Freud theorized that the mind was divided into three parts: id, ego and superego. The
function of the ego can be described as running interference between the id and the superego. It
mediates between the drives of the id and the need for self-preservation. The ego is responsible
for the development of the skills needed to function in the world, for example, impulse control,
perception, evaluation and judgment.
Id
Sigmund Freud theorized that the mind was divided into three parts: id, ego and superego. The id
is the part of the mind that contains one’s most basic and instinctive drives. It is governed by
sexual and aggressive desires and pleasure seeking. The contents of the id are entirely
unconscious; Freud stated that the goal of analysis is to uncover what is repressed in the id so
that, “where id was, there ego shall be.”
Superego
Sigmund Freud theorized that the mind was divided into three parts: id, ego and superego. The
superego can be thought of as the part of the mind that acts as the conscience. Its function is to
stop or punish behaviour that is unacceptable according the ego ideal, i.e., the standards, values,
and images of perfection that begin to develop in childhood, and which some psychoanalysts
believe to develop over a lifetime. Failure to live up to these standards results in feeling of gui.
Product of Cyclopentane + H2O(H+) gives No Reaction.It will simply F.pdf
Product of Cyclopentane + H2O(H+) gives No Reaction.It will simply Float on it.
No reaction
Solution
Product of Cyclopentane + H2O(H+) gives No Reaction.It will simply Float on it.
No reaction.
Of the variedtypes of IPC, sockets arout and awaythe foremostcommon..pdf
Of the variedtypes of IPC, sockets arout and awaythe foremostcommon. On any given platform,
there arprobably to be differenttypes of IPC that arquicker, except for cross-platform
communication, sockets arregardingthe sole game in city.
They were fancied in Berkeley as a part of the BSD flavor of UNIX operating system. They
unfold like inferno withthe web. With sensible reason — the mixture of sockets with INET
makes reprehensionabsolute machines round the world incrediblystraightforward (at least
compared to different schemes).
Creating a Socket
Roughly speaking, once you clicked on the link that brought you to the current page, your
browser did one thingjust like the following:
#create Associate in Nursing INET, STREAMing socket
s = socket.socket(
socket.AF_INET, socket.SOCK_STREAM)
#now connect withthe net server on port eighty
# - the traditionalcommunications protocol port
s.connect((\"www.mcmillan-inc.com\", 80))
When the connect completes, the socket s may beaccustomedsend outa call for participation for
the text of the page. a similar socket canbrowse the reply, so be destroyed. That’s right,
destroyed. shopper sockets arunremarkablysolely used for one exchange (or atiny low set of
sequent exchanges).
What happens within thenet server may be a bit additionalcomplicated. First, the net server
creates a “server socket”:
#create Associate in Nursing INET, STREAMing socket
serversocket = socket.socket(
socket.AF_INET, socket.SOCK_STREAM)
#bind the socket to a public host,
# and a widely known port
serversocket.bind((socket.gethostname(), 80))
#become a server socket
serversocket.listen(5)
A couple things to notice: we tend to used socket.gethostname() in order that the socket would
be visible to the surface world. If we tend to had used s.bind((\'localhost\', 80)) or
s.bind((\'127.0.0.1\', 80)) we\'d still have a “server” socket, however one that was solely visible
insidea similar machine. s.bind((\'\', 80)) specifies that the socket isaccessible by any address the
machine happens to own.
A second issue to note: low range ports arsometimes reserved for “well known” services (HTTP,
SNMP etc). If you’re kidding, use a pleasant high range (4 digits).
Finally, the argument to pay attention tells the socket library that we wish it to queue as several
as five connect requests (the traditional max) before refusing outside connections. If the
remainder of the code is written properly,that ought to be masses.
Now that we\'ve got a “server” socket, listening on port eighty, we will enter the mainloop of the
net server:
while 1:
#accept connections from outside
(clientsocket, address) = serversocket.accept()
#now do one thing with the clientsocket
#in this case, we\'ll fakethis can be a rib server
ct = client_thread(clientsocket)
ct.run()
There’s trulythree general ways thatduring which this loop might work - dispatching a thread to
handle clientsocket, producea replacementmethod to handle clientsocket, or structure this app to
use non-blocking socke.
C2O2 is a bidendate ligand &Cl - is a mono dendat.pdf
C2O2 is a bidendate ligand &Cl - is a mono dendate ligang. ---> The coordination
number of Co is 2*2 + 2 = 6 EDTA is a hexadentate ligang & Br is a mono dentate ligang. --->
The coordination number of Co is 6+1=7
Solution
C2O2 is a bidendate ligand &Cl - is a mono dendate ligang. ---> The coordination
number of Co is 2*2 + 2 = 6 EDTA is a hexadentate ligang & Br is a mono dentate ligang. --->
The coordination number of Co is 6+1=7.
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6a.The nucleotide excision repair or NER is mechanism that has cap.pdf
- 1. 6a. The nucleotide excision repair or NER is mechanism that has capacity to repair the damaged nucleotide bases which are formed due to covalent interaction with large hydrocarbons and due to formation of pyrimidine dimers (T-T, T-C or CC), this mechanism of DNA repair is present in bacteria, yeast and mammalian cells. The damaged bases are first cut out within a string of nucleotides, and replaced with new DNA using undamaged strand as a complementary strand with the assistance of DNA polymerase and DNA ligase. In prokaryotes, the enzymes that perform NER because of UV damage or pyrimidine dimers are UvrABC excinuclease and the UvrD helicase. The genes responsible for their formation are named as uvrA, uvrB, uvrC and uvrD. The UvrABC complex first recognizes the damaged part of DNA, followed by cleavage on both sides of the demage, this damaged part is released by UvrD helicase that unwinds DNA using ATP molecules. The gap so created is filled by new DNA using DNA polymerase and the nick so created is later joined with main DNA on either by DNA ligase. In eukaryotes, it has been reported that Pol II (polB ) and Pol IV (dinB) does not affect them after UV irradiation or dimmer formation and only affects Pol V (umuC) Solution 6a. The nucleotide excision repair or NER is mechanism that has capacity to repair the damaged nucleotide bases which are formed due to covalent interaction with large hydrocarbons and due to formation of pyrimidine dimers (T-T, T-C or CC), this mechanism of DNA repair is present in bacteria, yeast and mammalian cells. The damaged bases are first cut out within a string of nucleotides, and replaced with new DNA using undamaged strand as a complementary strand with the assistance of DNA polymerase and DNA ligase. In prokaryotes, the enzymes that perform NER because of UV damage or pyrimidine dimers are UvrABC excinuclease and the UvrD helicase. The genes responsible for their formation are named as uvrA, uvrB, uvrC and uvrD. The UvrABC complex first recognizes the damaged part of DNA, followed by cleavage on both sides of the demage, this damaged part is released by UvrD helicase that unwinds DNA using ATP molecules. The gap so created is filled by new DNA using DNA polymerase and the nick so created is later joined with main DNA on either by DNA ligase.
- 2. In eukaryotes, it has been reported that Pol II (polB ) and Pol IV (dinB) does not affect them after UV irradiation or dimmer formation and only affects Pol V (umuC)