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primase
DNA-dependent RNA polymerase for lagging strand Okazaki fragments
sliding clamp (Proliferating Cell Nuclear Antigen)
keeps polymerase from falling off DNA
topoisomerase
relieve DNA supercoiling
topotecan
blocks topoisomerase (results in genome fragmentation → cell death)
dyskeratosis congenita
telomerase dysfunction; mutations in TERT, TERC → graying hair, skin degeneration, bone marrow failure
origin licensing
MCM complex initiates replication at one OriC and immediately degrades
direct reversal of DNA damage
dealkylation (suicide repair proteins)
base excision repair
replaces single base mismatches (C→U, mC→T)
nucleotide excision repair
detects and replaces “bulky lesions” (UV dimerization of adjacent Ts)
xeroderma pigmentosum
severe photosenstivity due to defects in nucleotide excision repair
mismatch repair
mutS pathway recognizes slippage and repairs
non-homologous end joining
double-stranded break repair; quickly joins broken DNA ends backtogether
homologous repair
double stranded break repair; highly accurate repair system that uses template (can result in repeat expansion)
microdeletion syndrome
results from homologous repair of similar but nonhomologous regions
G0 phase
terminated cells withdraw from cell cycle
G1 phase
RNA and protein synthesis
S phase
DNA synthesis
G2 phase
RNA and protein synthesis continue (no DNA synthesis)
M phase
mitosis and cytokinesis
G1/S checkpoint
restriction point: cellular environment must be favorable for replication
S checkpoint
checks for DNA replication errors or damage
G2 checkpoint
checks for completion of DNA replication
M checkpoint
spindle checkpoint (APC/C will unpin chromatids)
Rb
brake on cell cycle progression
p53
activates p21
BCL2
prevents apoptosis
BAX/BAK
promotes apoptosis (forms channel in mitochondrial membrane)
amyloid is found
in between cells
tau is found
in cells