Random shit that I can't fucking remember to save my life Flashcards by Lucas Vandermyde | Brainscape

Q

DNA pol E

A

on the leading strand… synthesizes DNA

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Q

DNA pol Delta

A

on the lagging strand … fills in gaps

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Q

DNA pol Alpha

A

on the lagging strand

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Q

how are okazaki fragments put together?

A

FEN1 removes primer
DNA pol Delta fills in gap
DNA ligase (ATP dependent) seals gap

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Q

What is replicative senescence

A

when the telomerase activity is insufficient and the repeats are lost in each generation

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Q

What repeats are the telomeres?

A

GGGTTA

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Q

Depurination

A

Purine base is removed via hydrolysis of the n-glycosidic bond bw the base and the deoxyribose group

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Q

Deamination

A

amino group of purine or pyrimidine base is hydrolyzed
A-hypxanthine
G-xanthine
C- dU which is unnatural and bad

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Q

What does UV light do?

A

creates covalent linkage b/w adjacent pyrimidine bases… results in 2 major photoproducts that are bad
-p53 gene

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Q

What does methylation do to gene expression

A

silences it!

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Q

What repair mechanism is associated with Xeroderma pigmentosum?

A

Nucleotide excision repair

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Q

What disorder is caused by malfunctioning Transcription-coupled repair?

A

Cockayne syndrome

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Q

What are all the checkpoints in cell cycle?

A

G1-S
G2-M
Metaphase-Anaphase

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Q

in Meiosis, when does the cell become haploid?

A

after Meiosis I

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Q

Where does crossing over occur?

A

Prophase I of Meiosis

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Q

What protein will inhibit the CDK cyclin complex?

A

p27

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Q

What two enzymes P’s and deP’s the cyclin CDK complex respectively?

A

Wee kinase and CDC25 Phosphatase

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Q

What cyclin CDK complex gets us through the G1 checkpt?

A

CyclinD-CDK4

“ “- CDK6

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Q

What thing gets us from G1 into S phase?

A

CyclinE-CDK2

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Q

Which complex is the the one that gets us through S phase because it induces DNA synthesis?

A

CyclinA-CDK2

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Q

Which Complexes gets us through the G2 checkpoints?

A

CyclinA- CDK1
CyclinB- CDK1
btw, this gets us into mitosis so it’s kind of a big deal

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Q

Which checkpoint is the only one where CKI’s can’t inhibit the cyclin CDK complexes?

A

the G2 checkpoint

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Q

what happens at the metaphase-anaphase checkpoint?

A

all cyclin levels drop off

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Q

Wtf is p21?

A

a protein that is upregulated by p53 and it’s a CKI

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Q

What keeps p53 inactive?

A

MDM2, it’s kinda like Rb protein for EF2

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Q

What is p27?

A

a protein that binds cyclin cdk complex and stops it (by phosphorylating it???)

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Q

What is the difference between mosaicism and chimerism?

A

mosaic has genetically different cells with the same zygote while a chimera has genetically different cells with DIFFERENT zygotes

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Q

What is chimerism?

A

When fraternal twins fuse together… one of them could make the eggs for the girl and she could have a baby that’s not really genetically related to her

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Q

When does the zona pellucida begin to dissipate?

A

when the blastocyst implants into the uterus

-the fucking embryo hatches remember?!?!?!

Q

when does the cell change from totipotent to pluripotent?

A

when we change into a blastocyst

Q

when does the primitive streak form?

A

during week 3

Q

when does the differentiation of 3 primary germ layers form?

A

week 3

Q

what forms the mesoderm?

A

the notochord…. all vertebrates have it… we kinda build vertebrae around it

Q

What are the functions of the notochord?

A

rigid axis that embryo develops around
foundation where vertebral column will form
brings about formation of the neural tube

Q

What do GRK’s do?

A

they bind P the G protein and make arrestin (3rd intracellular loop) bind to it.. thereby inactivating it

Q

What do TF’s have to interact with to be effective?

A

both a promoter or enhancer region as well as RNA pol II

Q

What does RNA pol I make?

A

rRNA

Q

What does RNA pol II make?

A

pre mRNA

Q

What does RNA pol III make?

A

pre tRNA as well as the 5s rRNA

Q

What inhibits RNA pol II and III?

A

alpha- Amanitin

Q

What timeframe of development is critical for development?

A

Weeks 3-8, here the tetratogens from mom can fuck up the embryo

Q

Which of the TF’s we talked about can bind condesned chromatin during cell differentiation?

A

The Forkhead (fox) gene family

Q

What does BMP-4 do?

A

blocks the neural formation

-it gets inhibited in order to PERMIT neurulation in the ectoderm

Q

What signaling molecule has to bind to heparin sulfate to activate its receptors?

A

FGF’s

Q

What doe the Wnt family of signaling molecules do?

A

different things in different classes of vertebrates
bind to frizzled and LRP receptors on cell surface
signal transduced to beta catenin
that enters nucleus and forms complex to activate transcription of Wnt target genes

Q

What signaling molecules are good + regulators of growth?

A

SHH and FGF

Q

What signaling molecule is a good - regulator of growth?

A

BMP

Q

What does Retinoic Acid (metabolite of Vitamin A) do?

A

helps determine position along the embryonic anterior/posterior axis by serving as an intracellular signaling molecule that guides development of the posterior portion of the embryo
-it acts through HOX genes

Q

What are proto- oncogenes?

A

genes that are normally turned off

-they get GOF mutations to turn them into oncogenes and then cancer happens :(

Q

What does osteopontin do?

A

made by osteoblasts…. has a - effect on the number of HSC’s

Q

What is the only CFU that makes 2 different cell lineages?

A

the Granulocyte-Macrophage CFU: it makes neutrophils and macrophages

Q

Are HSC’s pluripotent?

A

yes apparently

Q

Are the Committed precursor cells pluripotent?

A

no, the are multipotent

Q

What are the 3 types of hematopoietic growth factors?

A

CSF’s, EPO and Thrombopoietin, and cytokines (interleukins)

-can be made outside the bone marrow as well as inside

Q

What makes HSC’s responsive to other cytokines in the fetal tissues and stromal cells?

A

Stem cell factor (SCF) also known as c-kit ligand

Q

What is prostaglandin E2?

A

it protects the stomach

Q

How are PG’s made?

A

Stimulus makes AA (PLA2) come out of membrane, COX changes it to a PG or Tx
-then PGD, E, and F and degraded by the lung OH-PGDH thing and the PGI and TxA are degraded by hydrolysis

Q

Which eicosinoid stilumates vasodilation and inhibits platlet aggregation?

A

PGI2

Q

Opposite of PGI2

A

TxA2

Q

What are all of the things that PGE2 affects?

A

Temp, uterine contraction, vasculature permeability, gut motility/protection, and pain

Q

What does PGI2 affect?

A

the renal and the vascular endothelium

Q

What G protein do PGE and I stimulate?

A

G alpha (S)

Q

What G ptn do PGF and TxA stimulate?

A

G q

Q

What does PGE and I do to smooth muscles?

A

makes them RELAX

Q

What does PGF and TxA do to smooth muscles?

A

makes them contract! Increase in Ca2+

Q

What were the two balancing Autocoids we talked about with the heart?

A

PGI2 and TxA

Q

Which COX is constitutive?

A

COX 1

-it responds to all of the physiological stimuli

Q

What are the consequences of a deficit in PGE2 and an Excess of PGE2?

A

deficit: ulcers
excess: diarreah and cramps

Q

What are PGE’s and PGF’s roles in birth?

A

PGE is to dilate the cervix

PGF is for uterine contraction

Q

What happens if there is a deficit of PG’s in the Kidney?

A

Na and H2O retention (edema)

Q

Which COX is good at responding to pathological stimuli?

A

COX 2… it’s a little more intense

Q

Why are omega threes so great?

A

the can replace AA in membrane with EPA and this promotes vasodilation and lowers BP and inhibits platlet aggregation