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24 Cards in this Set

  • Front
  • Back
What happens during cell recruitment
most cells are not cycling
-to get from G0 to G1, you need a stimulus and genes - immediate early genes, delayed early genes, late genes
-induced cell proliferation involves:

-initiated by growth factors
-requires cell adhesion/anchorage
-is accompanied by an orderly expression of certain defined gene sets
-culminates in DNA synthesis and cell division
Growth gene expression
-is temporally controlled throughout the cell cycle
-sequentially activated for a specific duration dependent on the stimulus
-length of activation depends onthe stimulus
What are the types of immediate early genes & what do they do?
1. mostly transcription factors
regulate genes involved in metabolic activities to culmintate in DNA synthesis

have to be anchor dependent to grow,
Name examples of early intermediate genes and what type they are
c-MYC - HLH (helix loop helix domain)

c-fos - leucine zipper
c-jun -leucine zipper
dyad symmetry motif
- motif needed for homodimerization fo immediate early Tx factors
-for instance Max-Max homodimer will bind a dyad symmetry motif
asymmetric motif
-required for immediate early gene Tx factor heterodimerization -
What are the two most important things to remember about tx factors - immediate early response genes
1. they work in PAIRS - homodimers and heterodimers

2. the N terminal region (the DNA binding domain is very important - its really stiff so that it can intercalcate into the DNA, and then there's a really important arginine that breaks the helix to give the stiff structure some flexibility
- a sequence on the DNA that the Tx factors recognize through their DBD
How is regulation of gene expression wtih Tx factors economical?
-because tx factors homodimerize (need dyad motif) and heterodimerize (need asymmetric motif)- this means yo can get a lot of different results with very few protein types
What are the parts of c-MYC?
- a TAD - a transcriptional activating domain - (not found in MAX)

-HLH - helix loop Helix -fascilitates DNA binding

-ZIP - region where Tx factor dimerizes with another Tx factor

-NLS to tell it to go to the nucleus
What are the parts of MAX
-no TAD, that's why Max-Max homodimers cannot activate Tx

-HLH - for DNA binding

-ZIP region for dimerization

-very small truncated protein
Who has HLH?

Who has Leucine zippers?
- c-Myc and Max have HLC

-c-jun & c-fos have leucine zippers
Why can't Max-Max homodimer activate Tx?
Max doesn't have a TAD domain, it needs c-MYC to activate Tx
Some examples of genes tat have E boxes?
Thymidylate Kinase (nucleotide synthesis)
Dihydrofolate reductase
Ornithine decarboxylase
Plasminogen activating factor
When is c-MYC activated constituitively?
-in diseased states like

-Burkitt's lymphoma (chromosomal rearrangement)
-cancer (breast cancer and small cell lung carcinoma)
-sporadic cancers
what are three mechanisms whereby c-MYC can be constituitively activated?
-chromosomal rearangement (Burkitts)
-gene amplification (breast carcinoma & SCL carsinoma)
-stimulated expression (sporadic cancer)
Burkitts lymphoma
-chromosomal translocation results in overproduction of c-MYC which results in cancer

-chromosome 8 & 14
importance of c-MYC

how does it regulate,

what does it regulate?
-TX factor that helps move cells out of G0 and into G1 so that proliferation can occur

-regulates lots of target genes through a hex a nucleotide motif (E-box) CACGTG

-regulates cell growth, proliferation, angiogenesis
hex a nucleotide motif (E-box) CACGTG
-c-MYC regulates lots of target genes through a hex a nucleotide motif (E-box) CACGTG
3 basic properties of HLH and Leucine zipper Tx factor family members
- function as homodimers and heterodimers
-regulate gene expression in a combinatorial manner
-are sequence specific DNA binding proteins
activated c-MYC state
Some key differences between MAX-MAx and MAX-Myc
- homodimers MAX are very stable,

-heterodimers MAx-Myc are unstable - so that they get ubiquinitated and degraded eventually,

the homeostatic balance favors repression (MAX-MAX)
Binding of MAX-MYC heterodimer
-causes activation of Tx
-histone acetylation
-DNA demethylation
Understanding cell growth control is critical to our perception of
-normal development
-wound healing
-diseases which are clinical problems