The document summarizes the cell cycle and its key phases. It discusses that the cell cycle consists of interphase, where the cell grows and duplicates its DNA, and mitosis, where the cell splits into two daughter cells. Interphase includes G1, S, and G2 phases, while mitosis includes prophase, metaphase, anaphase and telophase. Critical cell cycle checkpoints ensure DNA replication and chromosome separation occur with high fidelity. Cyclins and cyclin-dependent kinases control progression through the cell cycle phases.
Basic Cell cycle regulation suitable for undergraduate students.
This presentation has been started from the basics to enable easy understanding. It covers all the details of cell cycle regulation in yeast as well as higher eukaryotes.
this presentation has detailed information on cell cycle. it includes steps as well as how the proteins take part in cell cycle.
i have also added information on some experiments that were carried out.
happy studying :)
Basic Cell cycle regulation suitable for undergraduate students.
This presentation has been started from the basics to enable easy understanding. It covers all the details of cell cycle regulation in yeast as well as higher eukaryotes.
this presentation has detailed information on cell cycle. it includes steps as well as how the proteins take part in cell cycle.
i have also added information on some experiments that were carried out.
happy studying :)
A detailed description of molecular level of cell cycle. Its regulation by different checkpoints. The Structure and Function of MPF. Description of MPF discovery.
A cell cycle is a series of events that a cell passes through from the time until it reproduces its replica.
Howard and Pelc (1953) first time described it.
It is the growth and division of single cell into daughter cells and duplication (replication).
In prokaryotic cells, the cell cycle occurs via a process termed binary fission.
In eukaryotic cells, the cell cycle can be divided in two periods-
a) interphase
b) mitosis
Dr Zahid Azeem, working as Assistant Professor of Biochemistry at Azad Jammu and Kashmir Medical College, Muzaffarabad since 2012.
email; paym_zahid@live.com
cellcycle,cell cycle regulation,phases of cell cycle,cell injury,etiology of cell injury,mechanism of cell injury,apoptosisand necrosis,autophagy,cell death
A detailed description of molecular level of cell cycle. Its regulation by different checkpoints. The Structure and Function of MPF. Description of MPF discovery.
A cell cycle is a series of events that a cell passes through from the time until it reproduces its replica.
Howard and Pelc (1953) first time described it.
It is the growth and division of single cell into daughter cells and duplication (replication).
In prokaryotic cells, the cell cycle occurs via a process termed binary fission.
In eukaryotic cells, the cell cycle can be divided in two periods-
a) interphase
b) mitosis
Dr Zahid Azeem, working as Assistant Professor of Biochemistry at Azad Jammu and Kashmir Medical College, Muzaffarabad since 2012.
email; paym_zahid@live.com
cellcycle,cell cycle regulation,phases of cell cycle,cell injury,etiology of cell injury,mechanism of cell injury,apoptosisand necrosis,autophagy,cell death
a deeply explained process of cell division, for understanding it thoroughly. i tried to put in all the information i knew and collected. i hope it is helpful or you.
The cell cycle, or cell-division cycle, is the series of events that take place in a cell that cause it to divide into two daughter cells. These events include the duplication of its DNA (DNA replication) and some of its organelles, and subsequently the partitioning of its cytoplasm and other components into two daughter cells in a process called cell division.
here u will find every detail of cell cycle.
for more details ,visit @biOlOgy BINGE-insight learning
The sequence of events cell division, DNA replication and cell growth by which a cell duplicates its genome, eventually divides into two daughter cells is termed cell cycle.
The cell cycle, or cell-division cycle, is the series of events that take place in a cell leading to duplication of its DNA (DNA replication) and division of cytoplasm and organelles to produce two daughter cells.
The ability to recreate computational results with minimal effort and actionable metrics provides a solid foundation for scientific research and software development. When people can replicate an analysis at the touch of a button using open-source software, open data, and methods to assess and compare proposals, it significantly eases verification of results, engagement with a diverse range of contributors, and progress. However, we have yet to fully achieve this; there are still many sociotechnical frictions.
Inspired by David Donoho's vision, this talk aims to revisit the three crucial pillars of frictionless reproducibility (data sharing, code sharing, and competitive challenges) with the perspective of deep software variability.
Our observation is that multiple layers — hardware, operating systems, third-party libraries, software versions, input data, compile-time options, and parameters — are subject to variability that exacerbates frictions but is also essential for achieving robust, generalizable results and fostering innovation. I will first review the literature, providing evidence of how the complex variability interactions across these layers affect qualitative and quantitative software properties, thereby complicating the reproduction and replication of scientific studies in various fields.
I will then present some software engineering and AI techniques that can support the strategic exploration of variability spaces. These include the use of abstractions and models (e.g., feature models), sampling strategies (e.g., uniform, random), cost-effective measurements (e.g., incremental build of software configurations), and dimensionality reduction methods (e.g., transfer learning, feature selection, software debloating).
I will finally argue that deep variability is both the problem and solution of frictionless reproducibility, calling the software science community to develop new methods and tools to manage variability and foster reproducibility in software systems.
Exposé invité Journées Nationales du GDR GPL 2024
Toxic effects of heavy metals : Lead and Arsenicsanjana502982
Heavy metals are naturally occuring metallic chemical elements that have relatively high density, and are toxic at even low concentrations. All toxic metals are termed as heavy metals irrespective of their atomic mass and density, eg. arsenic, lead, mercury, cadmium, thallium, chromium, etc.
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Deep Behavioral Phenotyping in Systems Neuroscience for Functional Atlasing a...Ana Luísa Pinho
Functional Magnetic Resonance Imaging (fMRI) provides means to characterize brain activations in response to behavior. However, cognitive neuroscience has been limited to group-level effects referring to the performance of specific tasks. To obtain the functional profile of elementary cognitive mechanisms, the combination of brain responses to many tasks is required. Yet, to date, both structural atlases and parcellation-based activations do not fully account for cognitive function and still present several limitations. Further, they do not adapt overall to individual characteristics. In this talk, I will give an account of deep-behavioral phenotyping strategies, namely data-driven methods in large task-fMRI datasets, to optimize functional brain-data collection and improve inference of effects-of-interest related to mental processes. Key to this approach is the employment of fast multi-functional paradigms rich on features that can be well parametrized and, consequently, facilitate the creation of psycho-physiological constructs to be modelled with imaging data. Particular emphasis will be given to music stimuli when studying high-order cognitive mechanisms, due to their ecological nature and quality to enable complex behavior compounded by discrete entities. I will also discuss how deep-behavioral phenotyping and individualized models applied to neuroimaging data can better account for the subject-specific organization of domain-general cognitive systems in the human brain. Finally, the accumulation of functional brain signatures brings the possibility to clarify relationships among tasks and create a univocal link between brain systems and mental functions through: (1) the development of ontologies proposing an organization of cognitive processes; and (2) brain-network taxonomies describing functional specialization. To this end, tools to improve commensurability in cognitive science are necessary, such as public repositories, ontology-based platforms and automated meta-analysis tools. I will thus discuss some brain-atlasing resources currently under development, and their applicability in cognitive as well as clinical neuroscience.
DERIVATION OF MODIFIED BERNOULLI EQUATION WITH VISCOUS EFFECTS AND TERMINAL V...Wasswaderrick3
In this book, we use conservation of energy techniques on a fluid element to derive the Modified Bernoulli equation of flow with viscous or friction effects. We derive the general equation of flow/ velocity and then from this we derive the Pouiselle flow equation, the transition flow equation and the turbulent flow equation. In the situations where there are no viscous effects , the equation reduces to the Bernoulli equation. From experimental results, we are able to include other terms in the Bernoulli equation. We also look at cases where pressure gradients exist. We use the Modified Bernoulli equation to derive equations of flow rate for pipes of different cross sectional areas connected together. We also extend our techniques of energy conservation to a sphere falling in a viscous medium under the effect of gravity. We demonstrate Stokes equation of terminal velocity and turbulent flow equation. We look at a way of calculating the time taken for a body to fall in a viscous medium. We also look at the general equation of terminal velocity.
DERIVATION OF MODIFIED BERNOULLI EQUATION WITH VISCOUS EFFECTS AND TERMINAL V...
Cell biology and biochemistry slideshare 17 bcb0007
1. CELL BIOLOGY AND BIOCHEMISTRY
COURSE CODE : BIT1004
FACULTY : DR. GAYATHRI M
CELL CYCLE AND DIVISION
COMPILED BY :
SARATHCHANDRAN H
17BCB0007
DATE : 12.03.2018
2. INTRODUCTION :
• THE CELL CYCLE, OR CELL-DIVISION CYCLE (CDC), IS THE SERIES OF EVENTS THAT
TAKES PLACE IN A CELL LEADING TO ITS DIVISION AND DUPLICATION.
• IN CELLS WITHOUT A NUCLEUS (PROKARYOTIC), THE CELL CYCLE OCCURS VIA A
PROCESS TERMED BINARY FISSION. IN CELLS WITH A NUCLEUS (EUKARYOTES), THE
CELL CYCLE CAN BE DIVIDED IN TWO BRIEF PERIODS: INTERPHASE—DURING WHICH
THE CELL GROWS, ACCUMULATING NUTRIENTS NEEDED FOR MITOSIS AND
DUPLICATING ITS DNA—AND THE MITOSIS (M) PHASE, DURING WHICH THE CELL
SPLITS ITSELF INTO TWO DISTINCT CELLS, OFTEN CALLED "DAUGHTER CELLS".
• THE CELL-DIVISION CYCLE IS A VITAL PROCESS BY WHICH A SINGLE-CELLED
FERTILIZED EGG DEVELOPS INTO A MATURE ORGANISM, AS WELL AS THE PROCESS BY
WHICH HAIR, SKIN, BLOOD CELLS, AND SOME INTERNAL ORGANS ARE RENEWED.
3. PHASES OF CELL DIVISION:
THE CELL CYCLE CONSISTS OF FOUR
DISTINCT PHASES: G1 (GAP1) PHASE, S
PHASE (SYNTHESIS), G2 (GAP2) PHASE
(COLLECTIVELY KNOWN AS INTERPHASE)
AND M PHASE (MITOSIS). M (MITOSIS)
PHASE IS ITSELF COMPOSED OF TWO
TIGHTLY COUPLED PROCESSES: MITOSIS,
IN WHICH THE CELL'S CHROMOSOMES
ARE DIVIDED BETWEEN THE TWO
DAUGHTER CELLS, AND CYTOKINESIS, IN
WHICH THE CELL'S CYTOPLASM DIVIDES
IN HALF FORMING DISTINCT CELLS.
ACTIVATION OF EACH PHASE IS
DEPENDENT ON THE PROPER
PROGRESSION AND COMPLETION OF THE
PREVIOUS ONE. CELLS THAT HAVE
TEMPORARILY OR REVERSIBLY STOPPED
DIVIDING ARE SAID TO HAVE ENTERED A
STATE OF QUIESCENCE CALLED G0
PHASE.
4. • S PHASE
• INITIATION OF DNA REPLICATION IS INDICATION OF S PHASE; WHEN IT IS
COMPLETE, ALL OF THE CHROMOSOMES HAVE BEEN REPLICATED, AT THIS TIME
EACH CHROMOSOME HAS TWO (SISTER) CHROMATIDS. THUS, DURING THIS PHASE,
THE AMOUNT OF DNA IN THE CELL HAS EFFECTIVELY DOUBLED, THOUGH THE
PLOIDY OF THE CELL REMAINS THE SAME. RATES OF RNA TRANSCRIPTION AND
PROTEIN SYNTHESIS ARE VERY LOW DURING THIS PHASE. AN EXCEPTION TO THIS IS
PRODUCTION OF HISTONE PROTEIN, WHICH MOSTLY OCCURS DURING THE S
PHASE.[1]
• G2 PHASE
• AFTER S PHASE OR REPLICATION CELL THEN ENTERS THE G2 PHASE, WHICH LASTS
UNTIL THE CELL ENTERS MITOSIS. AGAIN, SIGNIFICANT BIOSYNTHESIS OCCURS
DURING THIS PHASE, MAINLY INVOLVING THE PRODUCTION OF MICROTUBULES,
WHICH ARE REQUIRED DURING THE PROCESS OF MITOSIS. INHIBITION OF PROTEIN
SYNTHESIS DURING G2 PHASE PREVENTS THE CELL FROM UNDERGOING MITOSIS.
5. G0 PHASE
• THE G0 PHASE IS A PERIOD IN THE CELL CYCLE IN WHICH CELLS EXIST IN A QUIESCENT STATE. G0
PHASE IS VIEWED AS EITHER AN EXTENDED G1 PHASE, WHERE THE CELL IS NEITHER DIVIDING NOR
PREPARING TO DIVIDE, OR A DISTINCT QUIESCENT STAGE THAT OCCURS OUTSIDE OF THE CELL CYCLE.
G0 IS SOMETIMES REFERRED TO AS A "POST-MITOTIC" STATE, SINCE CELLS IN G0 ARE IN A NON-
DIVIDING PHASE OUTSIDE OF THE CELL CYCLE. SOME TYPES OF CELLS, SUCH AS NERVE AND HEART
MUSCLE CELLS, BECOME POST-MITOTIC WHEN THEY REACH MATURITY (I.E., WHEN THEY ARE
TERMINALLY DIFFERENTIATED) BUT CONTINUE TO PERFORM THEIR MAIN FUNCTIONS FOR THE REST OF
THE ORGANISM'S LIFE. MULTINUCLEATED MUSCLE CELLS THAT DO NOT UNDERGO CYTOKINESIS ARE
ALSO OFTEN CONSIDERED TO BE IN THE G0 STAGE. ON OCCASION, A DISTINCTION IN TERMS IS MADE
BETWEEN A G0 CELL AND A 'POST-MITOTIC' CELL (E.G., HEART MUSCLE CELLS AND NEURONS), WHICH
WILL NEVER ENTER THE G1 PHASE, WHEREAS OTHER G0 CELLS MAY.
• G1 PHASE
• THE FIRST PHASE OF INTERPHASE IS G1 PHASE, FROM THE END OF THE PREVIOUS MITOSIS PHASE UNTIL
THE BEGINNING OF DNA REPLICATION IS CALLED G1 (G INDICATING GAP). IT IS ALSO CALLED THE
GROWTH PHASE. DURING THIS PHASE THE BIOSYNTHETIC ACTIVITIES OF THE CELL, WHICH HAD BEEN
CONSIDERABLY SLOWED DOWN DURING M PHASE, RESUME AT A HIGH RATE. THIS PHASE IS MARKED BY
SYNTHESIS OF VARIOUS ENZYMES THAT ARE REQUIRED IN S PHASE, MAINLY THOSE NEEDED FOR DNA
REPLICATION. DURATION OF G1 IS HIGHLY VARIABLE, EVEN AMONG DIFFERENT CELLS OF THE SAME
SPECIES.
6. PHASES OF CELL DIVISION :
• INTERPHASE:
• INTERPHASE IS THE PROCESS A CELL MUST GO THROUGH BEFORE
MITOSIS, MEIOSIS, AND CYTOKINESIS. INTERPHASE CONSISTS OF FOUR
MAIN STAGES: G1, S, G0, AND G2. G1 IS A TIME OF GROWTH FOR THE
CELL. IF THE CELL DOES NOT PROGRESS THROUGH G1, THE CELL THEN
ENTERS A STAGE CALLED G0. IN G0, CELLS ARE STILL LIVING BUT THEY
ARE PUT ON HOLD. THE CELLS MAY LATER BE CALLED BACK INTO
INTERPHASE IF NEEDED AT A LATER TIME. THERE ARE CHECKPOINTS
DURING INTERPHASE THAT ALLOW THE CELL TO BE EITHER
PROGRESSED OR DENIED FURTHER DEVELOPMENT. IN S PHASE, THE
CHROMOSOMES ARE REPLICATED IN ORDER FOR THE GENETIC
CONTENT TO BE MAINTAINED. DURING G2, THE CELL UNDERGOES THE
FINAL STAGES OF GROWTH BEFORE IT ENTERS THE M PHASE. THE M
PHASE, CAN BE EITHER MITOSIS OR MEIOSIS DEPENDING ON THE TYPE
OF CELL. GERM CELLS UNDERGO MEIOSIS, WHILE SOMATIC CELLS WILL
UNDERGO MITOSIS. AFTER THE CELL PROCEEDS SUCCESSFULLY
THROUGH THE M PHASE, IT MAY THEN UNDERGO CELL DIVISION
7. • PROPHASE[EDIT]
• PROPHASE IS THE FIRST STAGE OF DIVISION. THE
NUCLEAR ENVELOPE IS BROKEN DOWN, LONG
STRANDS OF CHROMATIN CONDENSE TO FORM
SHORTER MORE VISIBLE STRANDS CALLED
CHROMOSOMES, THE NUCLEOLUS DISAPPEARS, AND
MICROTUBULES ATTACH TO THE CHROMOSOMES AT
THE KINETOCHORES PRESENT IN THE
CENTROMERE. MICROTUBULES ASSOCIATED WITH
THE ALIGNMENT AND SEPARATION OF
CHROMOSOMES ARE REFERRED TO AS THE SPINDLE
AND SPINDLE FIBERS. CHROMOSOMES WILL ALSO BE
VISIBLE UNDER A MICROSCOPE AND WILL BE
CONNECTED AT THE CENTROMERE. DURING THIS
CONDENSATION AND ALIGNMENT PERIOD,
HOMOLOGOUS CHROMOSOMES MAY SWAP
PORTIONS OF THEIR DNA IN A PROCESS KNOWN AS
CROSSING OVER.
8. • METAPHASE[EDIT]
• METAPHASE IS THE STAGE IN CELL DIVISION
WHEN THE CHROMOSOMES LINE UP IN THE
MIDDLE OF THE CELL BY MTOCS ( MICROTUBULE
ORGANIZING CENTER) BY PUSHING AND PULLING
ON CENTROMERES OF BOTH CHROMATIDS
WHICH CAUSES THE CHROMOSOME TO MOVE TO
THE CENTER. THE CHROMOSOMES ARE STILL
CONDENSING AND ARE CURRENTLY AT ONE STEP
AWAY FROM BEING THE MOST COILED AND
CONDENSED THEY WILL BE. SPINDLE AND
SPINDLE FIBERS HAVE ALREADY CONNECTED TO
THE KINETOCHORES. AT THIS POINT, THE
CHROMOSOMES ARE READY TO SPLIT INTO
OPPOSITE POLES OF THE CELL TOWARDS THE
SPINDLE TO WHICH THEY ARE CONNECTED.
9. • ANAPHASE
• ANAPHASE IS A VERY SHORT STAGE OF THE CELL CYCLE AND OCCURS AFTER
THE CHROMOSOMES ALIGN AT THE MITOTIC PLATE. AFTER THE
CHROMOSOMES LINE UP IN THE MIDDLE OF THE CELL, THE SPINDLE FIBERS
WILL PULL THEM APART. THE CHROMOSOMES ARE SPLIT APART AS THE
SISTER CHROMATIDS MOVE TO OPPOSITE SIDES OF THE CELL.
• TELOPHASE
• TELOPHASE IS THE LAST STAGE OF THE CELL CYCLE. TWO CELLS FORM
AROUND THE CHROMATIN AT THE TWO POLES OF THE CELL. TWO NUCLEAR
MEMBRANES BEGIN TO REFORM AND THE CHROMATIN BEGIN TO UNWIND.
10.
11. • CYCLINS:
• CYCLINS ARE A GROUP OF PROTEINS THAT CONTROL THE PROGRESSION OF CELLS THROUGH
THE CELL CYCLE BY ACTIVATING CYCLIN-DEPENDENT KINASE (CDK) ENZYMES.CYCLINS WERE
DISCOVERED BY R. TIMOTHY HUNT IN 1982 WHILE STUDYING THE CELL CYCLE OF SEA
URCHINS.
• TYPES OF CYCLINS:
• THERE ARE SEVERAL DIFFERENT CYCLINS THAT ARE ACTIVE IN DIFFERENT PARTS OF THE CELL
CYCLE AND THAT CAUSE THE CDK TO PHOSPHORYLATE DIFFERENT SUBSTRATES.
• THERE ARE TWO GROUPS OF CYCLINS:
• G1/S CYCLINS – THESE CYCLINS ARE ESSENTIAL FOR THE CONTROL OF THE CELL CYCLE AT
THE G1/S TRANSITION, CYCLIN A / CDK2 – ACTIVE IN S PHASE. CYCLIN D / CDK4, CYCLIN D /
CDK6, AND CYCLIN E / CDK2 – REGULATES TRANSITION FROM G1 TO S PHASE.
• G2/M CYCLINS – ESSENTIAL FOR THE CONTROL OF THE CELL CYCLE AT THE G2/M TRANSITION
(MITOSIS). G2/M CYCLINS ACCUMULATE STEADILY DURING G2 AND ARE ABRUPTLY
DESTROYED AS CELLS EXIT FROM MITOSIS (AT THE END OF THE M-PHASE). CYCLIN B / CDK1 –
REGULATES PROGRESSION FROM G2 TO M PHASE.
• THERE ARE ALSO SEVERAL "ORPHAN" CYCLINS FOR WHICH NO CDK PARTNER HAS BEEN
IDENTIFIED. FOR EXAMPLE, CYCLIN F IS AN ORPHAN CYCLIN THAT IS ESSENTIAL FOR G2/M
12. Species Name Original name Size (amino acids) Function
Saccharomyces cerevisiae Cdk1 Cdc28 298 All cell-cycle stages
Schizosaccharomyces
pombe
Cdk1 Cdc2 297 All cell-cycle stages
Drosophila melanogaster Cdk1 Cdc2 297 M
Cdk2 Cdc2c 314 G1/S, S, possibly M
Cdk4 Cdk4/6 317 G1, promotes growth
Xenopus laevis Cdk1 Cdc2 301 M
Cdk2 297 S, possibly M
Homo sapiens Cdk1 Cdc2 297 M
Cdk2 298 G1, S, possibly M
Cdk4 301 G1
Cdk6 326 G1
16. CONCLUSION :
• THE CENTRAL EVENTS OF CELL REPRODUCTION ARE CHROMOSOME DUPLICATION,
WHICH TAKES PLACE IN S (SYNTHETIC) PHASE, FOLLOWED BY CHROMOSOME
SEGREGATION AND NUCLEAR DIVISION (MITOSIS) AND CELL DIVISION (CYTOKINESIS),
WHICH ARE COLLECTIVELY CALLED M (MITOTIC) PHASE.G1 IS THE GAP BETWEEN M
AND S PHASES, AND G2 IS THE GAP BETWEEN S AND M PHASES. IN THE BUDDING
YEAST, THE G2 PHASE IS PARTICULARLY EXTENDED, AND CYTOKINESIS (DAUGHTER-
CELL SEGREGATION) DOES NOT HAPPEN UNTIL A NEW S (SYNTHETIC) PHASE IS
LAUNCHED.
• FISSION YEAST GOVERNS MITOSIS BY MECHANISMS THAT ARE SIMILAR TO THOSE IN
MULTICELLULAR ANIMALS. IT NORMALLY PROLIFERATES IN A HAPLOID STATE. WHEN
STARVED, CELLS OF OPPOSITE MATING TYPES (P AND M) FUSE TO FORM A DIPLOID
ZYGOTE THAT IMMEDIATELY ENTERS MEIOSIS TO GENERATE FOUR HAPLOID SPORES.
WHEN CONDITIONS IMPROVE, THESE SPORES GERMINATE TO PRODUCE
PROLIFERATING HAPLOID CELLS.
17. REFERENCES :
• HARPER JW. A PHOSPHORYLATION-DRIVEN UBIQUITINATION SWITCH FOR CELL
CYCLE CONTROL. TRENDSCELL BIOL. 2002 MAR;12(3):104-7. PMID 11859016
• JUMP UP↑ BIOCHEMICAL SWITCHES IN THE CELL CYCLE
• JUMP UP↑ NOVAK, B.; TYSON, J.J. (1993), "NUMERICAL ANALYSIS OF A
COMPREHENSIVE MODEL OF M-PHASE CONTROL IN XENOPUS OOCYTE EXTRACTS
AND INTACT EMBRYOS", JOURNAL OF CELL SCIENCE 106(4): 1153, RETRIEVED 2009-
12-11
• ↑ JUMP UP TO:A B POMERENING, J. R., E. D. SONTAG, ET AL. (2003). "BUILDING A CELL
CYCLE OSCILLATOR: HYSTERESIS AND BISTABILITY IN THE ACTIVATION OF CDC2."
NAT CELL BIOL 5(4): 346-351.