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Cell Biology

Single-celled organisms grow and divide when essential nutrients are present and stop growing and dividing when nutrients are absent
Multicellular organisms generally isolated from environmental fluctuations
Differentiated cells stops dividing because the organs and tissues they form would not be properly organized
Hematopoietic stem cells continue producing new red and white blood cells and thus continue dividing
Epithelial cells lining organs continuously renewed
Non-dividing cells can be made to divide by specific signals example: lymphocytes are induced to proliferate by interaction with an appropriate foreign substance (antigen)
Cell cycle all of the events that occur from one mitotic division to the next, during which all of a cell's DNA is doubled and partitioned equally between two daughter cells
M phase includes the process of mitosis and cytokinesis
Mitosis partitions duplicated chromosomes into two nuclei; easily observed in a light microscope where the highly condensed chromosomes can be seen as well as cells undergoing division
Cytokinesis entire cell divides
Interphase period between divisions when cell grows and replicates its chromosomes; DNA replication occurs only during synthesis portion of interphase
Gap phases important functions in preparing cells for the synthesis and mitosis phases and providing checkpoints to halt the cell cycle if something goes wrong during synthesis and mitosis
G0 most cells in a fully developed animal stop proliferation, non-dividing state, remain here for weeks or lifetime; can re-enter cell cycle
Cdk cyclin-dependent protein kinases regulate entry of cells into S or M phase
Protein kinase enzyme that transfers a phosphate group from ATP to the hydroxyl group of specific serine, threonine, and tyrosine residues in proteins
Phosphorylation mechanism to control a protein's enzymatic activity, cell lifetime, binding to partners, and subcellular location
Cdks control initiation of DNA synthesis, mitosis, and cytokinesis; by themselves are inactive, must bind to a partner protein (cyclin) in order to become enzymatically active kinases
Cyclins 4 classes, each defined by specific stage of the cell cycle in which they bind their corresponding Cdk
G1-Cdk complex cyclin D (3 of this type in mammals) with Cdk4 and Cdk6
G1/S - Cdk complex cyclin E and Cdk2
S/Cdk complex cyclin A and Cdk2
M/Cdk complex cyclin B and Cdk1
Rb substrate for Cdks associates with transcription factor E2F preventing E2F from functioning; phosphorylation of Rb by Cdk releases it from E2F allowing E2F to stimulate expression of genes required for transition from G1 to S, including DNA replication genes
Cyclin production controlled transcription brings about synthesis of cyclins and controlled protein degradation brings about degradation of cyclins
Ubiquitin-proteasome cyclin degradation mediated by this; 76 amino acid protein joined by way of its C-terminus to the epsilon amino group of specific lysine residues in proteins
Origin of cancer genetic disease because requires alterations within specific genes; usually not inherited since alterations that cause it arise in somatic cells of an individual during its lifetime
Cancer cell properties display uncontrolled growth (cancer cells do not respond to signals that cause normal cells to stop growing and dividing), anchorage-independent; do not require growth factors
Normal cells anchorage dependent; secrete proteins that interact with surface receptors that signal a proper environment, immortal; numerous chromosomal aberrations
Cancer cells do not need growth factors the cell cycle can not respond to interaction of GFs with cell surface receptors that send regulatory signals into the cell
Aneuploidy cancer cells may lack large segments or even entire chromosomes and segments of different chromosomes may be joined together
Causes of cancer environmental effects that damage DNA
benzopyrene soot, tobacco, and cigarette smoke, converts metabolically to a derivative that covalently modifies Guanine residues in DNA
Tumor-suppressor genes normal genes that encode proteins which prevent proliferation; mutations that inactivate them cause LOF on proliferation and promote cancer
Oncogenes mutant versions of normal, proto-oncogenes encoding proteins that promote proliferation; mutations cause expression of proto-oncogenes at wrong time creating inappropriate signals to proliferate and promote cancer; GOF; cause genetic instability
Created by: ilk0710
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