Biochem Flashcards

1
Q

epinephrine (adrenaline)

A

receptor = GPCR(g-protein coupled receptor)

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2
Q

cortisol hormone

A

intracellular receptor

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3
Q

estradiol hormone

A

intracellular receptor

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4
Q

glucagon hormone

A

GPCR

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5
Q

growth hormone

A

tyrosine kinase-associated receptor

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6
Q

Insulin (hormone)

A

Receptor Tyrosine Kinase

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7
Q

Testosterone

A

Intracellular receptor

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8
Q

Epidermal Growth Factor (EGF)

A

Receptor tyrosine kinase (RTK)

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9
Q

platelet-derived growth factor (PDGF)

A

receptor tyrosine kinase (RTK)

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10
Q

Nerve growth factor (NGF)

A

Receptor tyrosine kinase (RTK)

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11
Q

Transforming growth factor-B

A

Serine/threonine receptor kinase

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12
Q

Nitric oxide (NO)

A

permanently binds guanylyl cyclase

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13
Q

Acetylcholine (ACh)

A

GPCR

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14
Q

Hormones that act on GPCRs

A

Epinephrine, glucagon, Acetylcholine

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15
Q

Hormones that bind to intracellular receptors

A
  • cortisol, estradiol, testosterone, Thyroid hormone (T3/Thyroxine), Vitamin D3
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16
Q

hormones that bind to RTKs (receptor tyrosine kinases)

A
  • insulin, EGF (epidermal growth factor), PDGF (platelet-derived GF), NGF (nerve GF)
17
Q

s and i GPCR signaling

A

Effector: adenylyl cyclase
2nd mess: cAMP (S - up, I- down)
Receptors: S - beta Adrenergic, glucagon, serotonin, vasopressin RsI - alpha adrenergic, Ach Rs

18
Q

q GPCR signaling

A

effector: PLC
2nd mess: IP3, DAG
Receptor: Ach (o)

19
Q

t GPCR signaling

A

effector: cGMP phosphodiesterase
2nd mess: cGMP (down)
Receptor: rhodopsin

20
Q

NO synthesis

A

substrate: argenine
product: citrulline and NO
3 NO synthases:
- Neuronal Constitutive NOS (nNOS)
- Endothelial constitutive NOS (eNOS): in smooth mm.
- Induced NOS (iNOS): in macrophages

21
Q

Phospholipase C cascade

A
initiated by RTK, 
activates Phosphoinositide (PI) pathway (w/ GPCRs)
--> increase cytosolic Ca2+ levels 
(boost signaling w/ Ca2+)
** directly makes DAG and Ins-1,4,5-P3
22
Q

Receptor Tyrosine Kinase (RTK) mech

A

set of 2 Rs on 2 intracellular proteins w/ tyrosine kinases.
Activate when ligands bind –> auto-phosphorylate and dimerize.
ligands: EGF, FGF, insulin (growth factors!)
pathways activated: Src, Phospholipase C, MAP kinase, PI-3K

23
Q

Insulin Receptor Substrate (“IRS”)

A

Insulin-specific receptor that binds to RTK (when RTK = activated),
=> docking station for mTOR, AkT, and MAPK

24
Q

AC (adenylyl cyclase) pathway

A

AC –(activate)–> cAMP,

2 cAMP –(activate)–> PKA –> (phosphorylate target proteins or cAMP Response Element ““CREBP””)

25
Q

protein kinase C

A

family of ser/thr kinases,
used in signaling cascades to phosphorylate target molecs.
(activated by DAG&Ca2+ from GPCRS, cGMP from NPRs)
promote cell proliferation

26
Q

Major cell cycle checkpoints

(4)

A
  1. restriction point (end of G1): to divide or not to divide?
  2. S phase checkpoint: is DNA is damaged, and not fixable?
  3. G2/M checkpoint: is replication completed?
  4. Spindle assembly checkpoint (M): are chromatids properly arranged on spindles?
27
Q

Clinical disease assoc. w/ problems with heme synth pathway…

  • ALA synthase
  • a-ALA dehydratase
  • uroporphyrinogen I synthase
  • uropophyrinogen decarboxylase
A
  1. ALA synthase (EtOH, barbituates, hypoxemia) => anemia
  2. ALA dehydratase (Lead toxicity) => Bx changes…
  3. Uroporphyrinogen I synthase (Acute intermittent pophyria) => urine darkens on standing
  4. Uroporphyrinogen decarboxylase (Porphyria cutanea tarda) => photosensitivity