Molecular - White Flashcards

1
Q

What makes cells different?

A

Differences in gene expression

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2
Q

What is the make up of a transcription factor?

A

N–DNA binding module — dimerization module — activation module —- regulatory module –C

Dimerization and regulatory are optional, DNA binding and activation are a must

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3
Q

Helix-turn-helix motif

A

Simplest; two alpha helices connect by a short chain of aas that make the “turn” at a fixed angle; longer helix portion = DNA binding module; helix-turn-helix proteins bind DNA as dimers

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4
Q

Zinc Finger domain

A

Includes Zn atom in the DNA binding motif; binds to major groove of DNA

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5
Q

Leucine supper motif

A

Two alpha helical DNA binding domains; dimerization through leucine zipper region; interactions b/w hydrophobic aa side chains (leucines) at every 7 aa down 1 side of alpha-helix –> forms zipper structure, grabs DNA like clothes pin

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6
Q

Helix loop helix domain

A

Consists of a short alpha chain connected by a loop to a second longer alpha chain. Can occur as homodimers or heterodimers. 3 domains: DNA binding domain, dimerization domain and activation domain.

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7
Q

What are the 2 ways in which RNA is de stabilzed?

A
  1. Decapping: exposed mRNA degraded from 5’ end (serves to protect RNA from RNA degrading enzymes)
  2. mRNA degraded from 3’ end through poly-A tail and into coding region
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8
Q

Post-translational processing and modifications

A

Required by proteins to be functional; proteins must fold into their 3D conformations helped by chaperones; bind cofactors

Ex: non-covalent interactions like folding and cofactor binding; covalent modification by glycosylation, phosphorylation, acetylation; binding to other subunits

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9
Q

Protea some

A

Apparatus that deliberately destroys aberrant protein

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10
Q

What are 2 examples of controls of gene expression?

A
  1. Methylation and genomic imprinting: what genes get expressed (or not) from mom and dad
  2. X-chromosome inactivation: even things out XX vs. XY - 2X chromosomes vs. 1 X chromosome
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11
Q

What are the 3 transition checkpoints in the cell cycle control system?

A

1: Start: G1 to S; cell commits to cell cycle entry and chromosome duplication
2. G2/M: move into chromosome alignment on spindle in metaphase
3. Metaphase to anaphase transition; trigger sister chromatid separation and cytokinesis

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12
Q

Cdks

A

Heart of cell-cycle control system; ACTIVITES of them rise and fall during cell cycle (not numbers); dependent on cyclins (must be bound to have protein kinase activity)

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13
Q

What are the proteins that regulate Cdks?

A

Cyclins

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14
Q

What is the property of Cdk when cyclin is not bound (inactive)?

A

The active site of Cdk is blocked by the T loop; binding cyclin causes the T loop to move out of the active site (Cdk partly active); phosphorylation of Cdk at T loop fully activates it (cave site)

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15
Q

What protein causes the phosphorylation of Cdk in the cave site to make it fully active?

A

CAK (Cdk activating kinase)

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16
Q

Condensin

A

At the end of S phase, chromosomes dramatically compact and sister chromatids become deistic separate units b/c of Condensin

17
Q

What activates APC/C to complete mitosis?

A

M-Cdk

18
Q

Force One in chromosome movement

A

Depolymerization: major force pulls the kinetochore and chromosome toward the spindle pole; depolymerization of the plus end of the microtubules drives the pulling of the kinetochore poleward

19
Q

Force 2 of chromosome movement:

A

Microtubules flux: microtubules are moved toward spindle poles while being dismantled at minus ends; tubulin added at plus end while being removed at minus end

20
Q

Force 3 of chromosome movement

A

Polar Ejection Force: kinesin 4, 10 motors on chromosomes interact w/ microtubules and transport chromosomes from poles; push pull phenomenon

21
Q

Procaspases

A

Inactive caspase precursor

22
Q

Executioner caspases:

A

Destroys actual target - executes apoptosis (caspase-3)

23
Q

What forms the apoptosome?

A

When cytochrome c is released from mitochondria, it binds to a protein called Apaf1 to form it.

24
Q

BH123 in apoptosis

A

BH123 proteins become activated, form aggregation in mitochondrial outer membrane and induce the release of cytochrome c - the apoptosome is formed

25
Q

Bcl2 proteins

A

Blocks BH123 from aggregated and allowing release of cytochrome c

26
Q

BH3-only protein

A

Inactivates Bcl2 to allow BH123 to aggregate

27
Q

IAPs

A

Block caspases

28
Q

Anti-IAPs

A

Neutralize the IAPs and liberate caspases

29
Q

Oncogenes

A

Over activity mutation: GOF; involves single mutation event and activation of gene causing proliferation (dominant); “gas pedal”

30
Q

Tumor suppressor genes

A

Under activity mutations; LOF; involve genes that inhibit growth. Mutation event: one gene - no effect; second mutation causes problems (recessive); “brakes”

31
Q

What are the different ways proto-oncogenes can be activated in to oncogenes?

A
  1. Deletion or point mutation in coding sequence
  2. Regulatory mutation
  3. Gene amplification
  4. Chromosome rearrangement
32
Q

What are the 2 major categories of tumor suppressor genes?

A
  1. Proteins that normally restrict cell growth and proliferation
  2. Proteins that maintain the integrity of the genome
33
Q

Hereditary Rb

A

LOF or deletion of 1 copy of Rb in every cell b/c defect is inherited so predisposed to be cancerous; but have 1 good copy of Rb; somatic event occurs which elimates the good copy and get a loss of heterozygosity

34
Q

Sporadic form of Rb

A

Cancerous cells have both copies of Rb mutated; 2 hit hypothesis; Rb is a regulator of the cell cycle

35
Q

What mutation is important in colorectal cancer?

A

Loss in APC mutation - LOF; APC is a tumor suppressor gene