Molec Bio White Flashcards

Question

committee

Answer 1

gene activation

Answer 2

1. decapping from 5' end 2. mRNA degaded fomr 3' end through poly-A tail ^^ both act like a timer

Answer 3

need proteins to be FUNCTIONAL must fold into 3D conformation chaperones have fold correctly

Answer 4

destroys protein via ubiquitin one E1 activations 30 E2 activations 100s E3 accesory proteins

Answer 5

methylation/genomic imprinting: what genes get expressed (or not) from mom/dad X chromosome inactivation: even things out, 2X vs 1X chromosome (XX, XY)

Answer 6

1. Start: commits to entry and chromosome duplication 2. G2/M: chromosome alignment (is all DNA replicated) 3. metaphase to anaphase transition: are all chromosomes attached to spindle

Answer 7

HEART OF CELL CYCLE CONTROL SYSTEM - activities of Cdks change, NOT LEVELS - without cyclins, not active

Answer 8

levels vary | regulate and activate Cdk

Answer 9

anaphase promoting complex initiates metaphase to anaphase transition -targets S-cyclin and M-cyclin -activated by M-Cdk to complete mitosis

Answer 10

inactive: without cyclin or CAK (T loop blocks active site) partially active: cyclin bound (removes T loop from site) fully active: CAK phosphorylates cdk at T loop

Answer 11

inhibits Cdk activity by phosphorylating roof site

Answer 12

increase cdk activity by dephosphorylating roof site that was previously phosphorylated

Answer 13

cdk inhibitory protein (inhibits cyclin-cdk complex) | -used for control of G1/S-Cdk and S-Cdk in early cycle

Answer 14

causes chromosome condensation and resolution

Answer 15

APCC adds ubiquitin --> destroys securin --> separase now active --> cleaves cohesin --> sister chromatids come apart --> anaphase begins cohesin: holds sister chromatids together securin :protects cohesion (inhibitor of separase) separase: enzyme that cleaves cohesin

Answer 16

programmed cell death | -important in development of mature forms

Answer 17

inactive precursor for caspases

Answer 18

activates downstream caspases

Answer 19

destroys actual targets ( executes apoptosis) | esp. caspase 3

Answer 20

cytochrome c is released from mitochondria --> binds Apaf1 --> forms apoptosome

Answer 21

pro-apoptotic | activated --> forms aggregation in mit outer mem --> induce release of cyt C --> apoptosome formed

Answer 22

regulate intrinsic apoptosis - anti-apoptotic protein (inhibits apoptosis) - controls release of cyt C into cytosol

Answer 23

pro-apoptotic | inhibits BCl2 protein from inhibiting release of cyt C

Answer 24

inhibitor of apoptosis (good thing) | binds/inhibit caspases and prevents them from autoactivating

Answer 25

neutralize IAP and liberate caspases if apoptotic signal causes release of anti-IAPs from mit to block IAP activity --> executioner caspases activated when IAPs blocked

Answer 26

disease of aging

Answer 27

overactivity mutation gain of function single mutation --> proliferation

Answer 28

underactivity mutation loss of function needs two mutations to cause problems (recessive)

Answer 29

deletion or point mutation in coding sequence regulatory mutation gene amplification chromosome rearrangement ALL ARE DOMINANT

Answer 30

1. proteins that normally restrict cell growth and proliferation 2. proteins that maintain integrity of genome

Answer 31

both eyes affected. 40% (more common) one copy of Rb is fucked up, you still have one good gene somatic event occurs -- eliminates good copy and forms tumor loss of heterozygosity

Answer 32

``` one eye affected, no family history 60% (more rare) no mutation of Rb both copies of Rb mutated first Tb mutation then second ```

Answer 33

precursor of colorectal Ca 10 years can develop into adenoma

Answer 34

majority: loss of Apc (tumor suppressor gene) then loss of p53 then activation of K-Ras

Answer 35

mardi gras beads | determine shape of cells surface and necessary for whole cell locomotion, secretion, endocytosis

Answer 36

slinky tube like structure determine position of organelles directs intracellular transport

Answer 37

grinders in building mechanical strength resist mechanical stress formation of hair and fingernails

Answer 38

actin monomer contains binding site for ATP or ADP | arranged head to tail --> generates structural polarity

Answer 39

``` formation of microtubules heterodimer of a tubulin and b tubulin with noncovalent bonds binding site for GTP (+) end = growing end (-) end = shrinking end ```

Answer 40

leads to hemolytic anemia | hereditary spherocytosis

Answer 41

primary component of RBC cytoskeleton tight capillary spaces -if defective, Hereditary spherocytosis

Answer 42

``` bacteria that invades intestine attaches to receptors on RBC behavior based on actin cytoskeleton faster than submarine involves ARP complex (accessory protein) cause branching actin ```

Answer 43

``` severe, loss ability to walk by 12 y.o dead by 20s X linked recessive lack of dystrophin clinical: necrosis of muscle, replace with CT or fat kids: Gower Maneuver ```

Answer 44

- function: provide stability to muscle cell membrane during cycles of contraction and relaxation - 4 functional domains - cysteine rich and C terminus domains

Answer 45

``` mild lose ability to walk by 16 y.o heart failure X linked recessive has dystrophin by abnormal quantity/size ```

Answer 46

``` ragged red fibers maternally inherited self replicated higher mutation than nuclear threshold effect need a mutation AND threshold effect affects brain/CNS, heart, skeletal m ```

Answer 47

mixture of normal and mutant mitochondria

Answer 48

myoclonic epilepsy ataxia ragged red fibers majority: mutation due to A => G

Answer 49

mutation in tRNAleu seizures most common ragged red fibers

Answer 50

``` retinitis pigmentosa cardiac conduction abnormality cerebellar ataxia majority: due to mtDNA rearrangements ragged red fibers ```

Answer 51

ragged red fibers | ptosis

Answer 52

only affects optic n no muscle involvement vision loss mutation in complex 1 proteins