Cell biology and cellular processes vol 2 issue 2

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Amity University, Lucknow (U.P.),
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Calcutta University Institute of Post Graduate
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West Virginia State University Research &
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School of Studies in Botany, Jiwaji University,
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CBIT, Hyderabad, India
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1. Role of Fungus and Mycotoxins in the Genesis of the Breast Carcinoma
A. Ravi Shankar, R. RajKumar, K. Rutu Raj, M. Guru Prasad 1
2. Overview of Cell Signaling
Anuradha Chaudhary 9
3. New Switch Decides Between Genome Repairs, Death of Cells: A Report
Shaina Chaudhary 16
4. Structure of an Anti-CRISPR Protein
Anuradha Chaudhary 17
5. Short Communication: How HIV Destroys Immune Cells?
Manjit Singh 22
Contents

IJCBCP (2016) 1-8 © JournalsPub 2016. All Rights Reserved Page 1
International Journal of Cell Biology and Cellular Processes
Vol. 2: Issue 2
www.journalspub.com
Role of Fungus and Mycotoxins in the Genesis of the Breast
Carcinoma
A. Ravi Shankar, R. RajKumar, K. Rutu Raj*, M. Guru Prasad
Department of Microbiology, Kamineni Academy of Medical Sciences and Research Centre, Telangana, India
ABSTRACT
The commonest cancer in the world affecting the women after cervical carcinoma is the
breast cancer. The etiology for the genesis and progression of breast cancer includes
mutations and infectious agents including oncogenic viruses and fungi. The role of oncogenic
viruses in the formation of breast carcinoma is known. We reviewed the possible role of the
fungi or mycotoxin and carcinogenic mechanism in breast cancer formation.
Keywords: BRCA1, BRCA2, mycotoxins, TGF-2
INTRODUCTION
Fungi are the large group of eukaryotic
organisms including yeasts, molds as well
as edible mushrooms. These organisms
were different from others in having the
presence of chitin in their cell wall. Fungi
were very abundant in nature and spread
worldwide and act as symbionts,
nonpathogenic and pathogenic organisms.
They play an important role in the organic
matter decomposition in nature,
fermentation of the various food products,
production of antibiotics etc. On the other
hand fungi acts as major pathogens or the
agents causing disease in humans, and it is
collectively termed as the mycoses,
similarly the exposure of skin, or diet to
the toxic fungal metabolites leads to a
condition termed as
mycotoxicoses.[1].
These fungi or
mycotoxins termed as hidden killers, they
cause a number of infections in numerous
organs of the body. It includes
dermatophytes causing athletes foot, or
infection to nails.[1]
The invasive fungal
infections are mainly caused by
Cryptococcus, Candida, Aspergillus sp.
The fungal pathogens such as
Cryptococcus sp. were classified as the
primary pathogen which causes disease
leading to the development of subclinical
disease.[2]
These opportunistic pathogens incite
disease in patients with impaired immune
system. The virulence factors which
contribute for the development of the
mycoses includes the adherence to the
tissues by the fungus involving the a cell
wall molecule adhesion, which resist the
physical clearing the fungus in the
humans, for example Histoplasma
capsulatum and Candida albicans adhere
to various host surfaces, avoid being
washed out and initiates the onset of
hematogenous infections.[2]
The other mechanism includes the
presence of penetration and dissemination
factors. The Aspergillus fumigatus has an
ability to penetrate the blood vessels and
disseminate through blood.[3]
The necrotic
enzymes produced by the fungus such as
extracellular proteinase produced by the C.
albicans, Aspergillus sp. allow the fungus
to overcome structural barriers. The other

IJCBCP (2016) 9–15 © JournalsPub 2016. All Rights Reserved Page 9
Vol. 2: Issue 2
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Overview of Cell Signaling
Anuradha Chaudhary
Department of Biotechnology, Lovely Professional University, Punjab, India
Cells regularly convey utilizing chemical
signals. These chemical signs, which are
proteins or different molecules produced
by a sending cell, are regularly discharged
from the cell and discharged into the
extracellular space. There, they can float –
like messages in a bottle – over to
neighboring cells.
 Sending cell: this cell secretes a ligand
 Target cell: this cell has a receptor that
can tie the ligand. The ligand ties to
the receptor and triggers a signaling
cascade inside the cell, prompting to a
response.
 Non target cell: this cell does not have
a receptor for the ligand (however it
might have different sorts of
receptors). The cell does not see the
ligand and in this manner does not
react to it.
Not all cells can "hear" a specific chemical
message. In order to detect a signal (that
is, to be a target cell), a neighbor cell must
have the correct receptor for that signal.
At the point when a signaling molecule
ties to its receptor, it adjusts the shape or
movement of the receptor, triggering off a
change within the cell. Signaling particles
are regularly called ligands, a general term
for molecules that predicament
particularly to different molecules, (for
example, receptors).
The message conveyed by a ligand is
frequently handed-off through a chain of
chemicals messengers inside the cell [1].
At last, it prompts to an adjustment in the
cell, for example, modification in the
movement of a gene or even the
acceptance of an entire procedure, for
example, cell division. In this manner, the
first intercellular (between-cells) signal is
changed into an intracellular (inside cell)
signal that triggers a reaction.
Types of Signaling
Cell-cell signaling includes the
transmission of a signal from a sending
cell to a receiving cell. Notwithstanding,
not all sending and receiving cells are
nearby neighbors, nor do all cell pairs
exchange signals in the same way.

Vol. 2: Issue 2
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New Switch Decides Between Genome Repairs, Death of Cells: A
Report
Shaina Chaudhary
Department of Microbiology, Lovely Professional University, Punjab, India
The genetic information of each cell is
encoded in the sequence of the DNA double
helix. Double strand breaks up the DNA,
which can be instigated by radiation, are a
dangerous threat to the cells, and if not
appropriately repaired can prompt to cancer.
Damaged cells need to choose whether the
breaks can be settled or whether they ought
to be evacuated by a cellular suicide
program called "apoptosis" before starting
cancer.
The genetic information of each cell is
encoded in the sequence of the DNA double
helix. Double strand breaks up the DNA,
which can be initiated by radiation, are a
dangerous danger to the cells, and if not
appropriately repaired can prompt to cancer.
Damaged cells need to choose whether the
breaks can be settled or whether they ought
to be evacuated by a cellular suicide
program called "apoptosis" before starting
cancer.
Björn Schumacher, one of the senior
authors, clarifies: "Inside seconds after an
unsafe episode, diverse instruments begin.
Schizophrenically, the cells begin repairing
and in preparing for apoptosis. We
recognized an uncharacterized system that
incorporates signals from the continuous
repair handle and the cell death machinery.
A protein called UFD-2 frames expansive
edifices at the breaks and verifies whether to
proceed with the repair or whether it's time
to die." Simultaneously, UFD-2 is a point of
intersection that both gets and gives signals.
The tests were performed with the nematode
Caenorhabditis elegans. "For our research
we utilized diverse strains of C. elegans,
including wild sort and genetically modified
ones. They were presented to ionizing
radiation to instigate double strand breaks
and afterward analyzed," says Leena
Ackermann, lead author of the review.
Schumacher includes: "The outcomes are
imperative to additionally see how and why
a cell chooses to repair or to die. Is the repair
as yet continuous and effective or is
apoptosis essential? Cells lacking UFD-2
neglect to experience apoptosis. In people
such a circumstance could prompt to a
higher danger of a damaged cell turning into
a cancer cell."
All the proteins that have an influence in this
mechanism can be found in humans also,
and the discoveries could be exceptionally
applicable to better seeing how DNA
damage prompts to cancer. DNA damage is
likewise an imperative driver of the aging
process. Despite the fact that apoptosis
protects from cancer, excessive cell death
can prompt to tissue degeneration and aging.
The senior author Thorsten Hoppe initially
distinguished UFD-2 as a key regulator of
protein degradation. Here, UFD-2 frames
administrative focuses that facilitate DNA
repair and cell death. Hoppe seeks after
coming about advances in tumor therapy:
"The information we picked up from this
review gives new points of view to fighting
cancer pharmaceutically. It may be
conceivable to control the very much
balanced process of apoptosis and protein
degradation to make clearance of tumor cells
more proficient."

Vol. 2: Issue 2
www.journalspub.com
Structure of an Anti-CRISPR Protein
Anuradha Chaudhary*
Department of Biotechnology, Lovely Professional University, Punjab, India
ABSTRACT
Bacterial CRISPR–Cas adaptive immune systems utilize small guide RNAs to protect against
phage infection and invasion by outside genetic components. We heretofore showed that a
get-together of Pseudomonas aeruginosa phages encode against CRISPR proteins that
inactivate the type I-F and I-E CRISPR–Cas frameworks using particular mechanisms. Here,
we present the three-dimensional structure of a hostile to CRISPR protein and guide a
valuable surface that is essential for its powerful inhibitory action. The connection of the
counter CRISPR protein with the CRISPR–Cas complex through this utilitarian surface is
proposed to keep the binding of target DNA.
Keywords: bacteria, DNA, RNA
INTRODUCTION
Phage predation is a major selective
pressure on bacterial populaces, and
bacteria have advanced an evolved an
adaptive immune system, known as
CRISPR–Cas, to shield against them.
CRISPR loci are included palindromic
repeats sequences blended with novel short
spacer districts that are regularly identical
to phage and plasmid deoxyribonucleic
acid (DNA) After transcription, CRISPR
ribonucleic corrosive (RNA) is prepared
and complexed with Cas proteins to frame
a genome reconnaissance system guided
by the sequence of the spacer RNA.
Sequences particular authoritative by this
complex to an invading phage genome
targets it for degradation. AcrF1, is a
strong inhibitor of the type I-F CRISPR–
Cas system of P. aeruginosa. AcrF1
hinders the DNA- binding activity of the
reconnaissance complex of this system
(called the Csy complex) by
communicating with the Csy3 subunit6 [1,
2]. Using site-directed mutagenesis,
recognize a practical surface through
which it intervene its hostile to CRISPR
movement. The inactivation of the type I-F
CRISPR–Cas system by AcrF1 was
observed to be reliant on tight official to
the Csy complex.
LOCUS STRUCTURE
Repeats and Spacers
CRISPR repeats extend in size from 24 to
48 base pairs. They more often than some
dyad symmetry, inferring the arrangement
of an auxiliary structure, for example, a
hairpin, yet are not really palindromic.
Repeats are isolated by spacers of
comparable length. Some CRISPR spacer
sequences precisely coordinate
arrangements from plasmids and phages,
although some spacers coordinate the
prokaryote's genome (self-targeting
spacers) [3]. New spacers can be included
quickly as a major aspect of the immune
response to phage infection.
Cas Genes and CRISPR Subtypes
Small clusters of cas genes are frequently
situated alongside CRISPR repeat-spacer
arrays. Similar genomics identified
multiple cas genes; an underlying analysis

Vol. 2: Issue 2
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Short Communication: How HIV Destroys Immune Cells?
Manjit Singh
Department of Biotechnology, DAV College, Punjab, India
HIV leads to AIDS principally because the
virus destroys essential immune cells
called CD4 T cells, but precisely how
these cells are killed has not been clear.
Two papers written by same G. Doitsh et
al. and K. M. Monroe et al. reveal the
molecular components that cause the death
of most CD4 T cells in lymphoid tissues,
the main reservoir for such cells, during
infection.
Two research groups led by Warner
Greene at the Gladstone Institutes in San
Francisco have exhibited that by far most
of CD4 T cells in lymphoid tissues despite
their ability to resist full infection by HIV,
respond to the presence of viral DNA by
relinquishing themselves by means of
pyroptosis – a highly inflammatory form
cell death that lures more CD4 T cells to
the area, in this manner making an endless
loop that eventually wreaks havoc on the
immune system.
"It's truly elegant science," said Anthony
Fauci, director of the National Institute for
Allergy and Infectious Diseases at the
National Institutes of Health (NIH) in
Bethesda, Maryland, who was not included
in the research. "It goes far to clarifying
what has been a puzzle for all intents and
purposes 30 years."
Richard Koup, who drives the
immunology lab at the Vaccine Research
Center at the NIH, concurred: “For a
considerable length of time we have
recently said ‘HIV infects the cells and
kills them,’ however it's obviously more
complicated than that. These papers begin
to depict the numerous diverse
components that HIV may need to
slaughter CD4 T cells” [1].
“This cell-death pathway interfaces the
two signatures of HIV Research Center
that is, CD4 T cell-depletion and chronic
inflammation surprisingly,” included
Greene, who coordinates the Gladstone
Institute of Virology and Immunology.
Besides, existing anti-inflammatory can
hinder the pathway, raising the possibility
of new therapies that objective the host
reaction as opposed to the virus.
The death of CD4 T cells amid HIV
infection has by and large been credited to
plain old apoptosis, or customized cell
death. Issue is, most reviews have
concentrated on active cells in the blood,
which are “productively infected “by HIV,
implying that the virus has incorporated
with host-cell genome and can make
duplicates of itself. In a recent report,
Greene and his associates demonstrated
that 95 percent of CD4 T cells in lymphoid
tissue, by differentiation, are bystander
cells that are " abortively infected "– the
virus penetrates however can't coordinate
or repeat. To better comprehend HIV
pathogenesis, Greene tried to make sense
of how this specific populace of immune
cells dies during HIV infection.
G. Doitsh et al. looked at human spleen
and tonsil tissue refined in the lab and
spiked with HIV. The scientists found that
when the virus productively infects the
couple of permissive CD4 T cells present,
death happens through apoptosis
intervened by a protein called caspase-3.
Be that as it may, when HIV abortively

Cell biology and cellular processes vol 2 issue 2

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