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Biochemistry > Yokomori > Flashcards

Yokomori Flashcards

0
Q

What are the two major mechanisms of reversible transmission?

A

phosphate transfer (phosphorylation and dephosphorylation) and nucleotide exchange (replacing a GDP with a GTP via hydrolysis)

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1
Q

What are the different types of cell to cell signalling?

A

paracrine, autocrine, endocrine, synaptic, gap junction

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2
Q

What are the 3 types of cell surface receptor?

A

Ion-channel-linked
G-protein-linked
Enzyme-linked

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3
Q

_____ hormones can homodimerize, while ________ hormone receptors must heterodimerize with their common binding partner ____.

A

Steroid; non-steroid; RXR

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4
Q

What are the major steroid (Type 1) nuclear receptors? What are the major non-steroid (Type 2) nuclear receptors?

A

Steroid: glucocorticoids (GR), mineralocorticoids (aldosterone), sex steroids [estrogen (ER), androgen (AR)]
Non-steroid: retinoid/retinoic acid (RAR, RXR*), thyroid (TR), Vitamin D3 (VDR)

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5
Q

What is the difference between a NISS and a MISS?

A

Nuclear-initiated steroid signal: Steroid binds its receptor and steroid+receptor complex binds a DNA regulatory sequence, becoming a trans-acting transcription factor.
Membrane-initiated steroid signal: Steroid binds receptor on outside surface of cell, activating other kinases and downstream targets.

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6
Q

Histone _____ serves as a coactivator and histone ____ serves as a corepressor.

A

acetyltransferase (HAT), deacetylase (HDAC)

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7
Q

How is the glucocorticoid (GR) pathway regulated?

A

HPA Axis: The HYPOTHALAMUS secretes vasopressin (AVP) and corticotropin releasing factor (CRF) under the control of the hippocampus and the amygdala. AVP and CRF cause the ANTERIOR PITUITARY to release adrenocorticotropic hormone (ACTH). ACTH stimulates production of glucocorticoids by the ADRENAL CORTEX.

AVP/CRF (hypothalamus) –> +ACTH (anterior pituitary) –> +Glucocorticoids (adrenal cortex)

Regulated by negative feedback of glucocorticoids on synthesis of ACTH and CRF.

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8
Q

What is Cushing sydrome?

A

hypercortisolism (too much cortisol, a glucocorticoid) caused by adrenal hyperplasia and other defects that result in overproduction of ACTH or cortisol.

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9
Q

Aldosterone is a _______ hormone.

A

mineralocorticoid (activates MR)

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10
Q

MR is expressed in the ____ and causes resorption of ____ and ____ back into the blood stream, which prevents _____ but also raises _____.

A

kidney, Na+, water, dehydration, blood pressure

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11
Q

_____ can occur secondary to a defect in the androgen receptor (AR) gene.

A

Androgen insensitivity syndrome (AIS)

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12
Q

Kennedy’s disease (Spinal and bulbar muscular atrophy (SBMA)) and prostate cancer involve defects in what pathway?

A

androgen receptor (AR)

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13
Q 
Type 2 (non-steroid) receptors heterodimerize with \_\_\_ and are
constitutively bound to their DNA response elements in the absence of their ligand. In the absence of ligand, the receptors serve as transcriptional \_\_\_\_\_\_\_, and \_\_\_\_ transcription after binding their ligand.
A

RXR, repressors, activate

*Activation does NOT require the RXR LIGAND (9-cis retinoic acid). Type 2 receptors will heterodimerize with the RXR receptor (repressor state), and become active (dissociate from RXR) after binding their own ligands.

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14
Q

Which organs are involved in the thyroid hormone receptor (TR) pathway?

A

Hypothalamus: thyrotropin-releasing factor (TRF)
Anterior pituitary: thyroid-stimulating hormone (TSH)
Thyroid: thyroxine (T4), triiodothyronine (T3) - stimulate metabolism in almost every tissue of the body

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15
Q

What is Graves’ Disease? What can this lead to if poorly managed?

A

hyperthyroidism; thyroid storm/thyrotoxic crisis (life-threatening hypermetabolic state)

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16
Q

What causes hypocalcemic vitamin D-resistant rickets? How is this different than classic rickets?

A

Vitamin D receptor (VDR) mutation; classic rickets is caused by vitamin D deficiency not by genetic mutation

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17
Q

Chromosomal translocation resulting in abnormal RAR fusion proteins is a cause of which disease?

A

acute promyelocytic leukemia (AML)

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18
Q

Which receptors serve as the major sensor of dietary cholesterol in the liver?

A

Liver X receptor (LXR), binds oxysterol which is produced in the liver when cholesterol is abundant

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19
Q

Which receptor is involved in regulation of cytochrome P450 genes? What do these genes do?

A

Pregnane X receptor (PXR), detoxification/metabolism of xenobiotics (drugs)

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20
Q

What type of receptor are LXR and PXR?

A

orphan receptors (sensors functioning in homeostasis)

21
Q

Peroxisome proliferator-activated receptors (PPARs) are lipid sensors who usually bind ____ as ligands. What are two synthetic PPAR ligands?

A

fatty acids; fibrates, TZDs

22
Q

Drugs such as Metoprolol are _____. What effect do they have?

A

β1-adrenergic receptor-selective antagonists (beta blockers); lower heart rate in tx of cardiac arrhythmias and angina

23
Q

What type of drug is Albuterol? What effect does it have?

A

β2-receptor agonist; relaxes smooth muscle of bronchial passages, thereby opening them

24
Q

In general terms, how are GPCRs activated?

A
  1. A receptor protein binds its ligand in the extracellular space
  2. This recruits the inactive, GDP-bound G protein trimer
  3. The ligand+receptor complex and the GDP+G protein complex interact, GDP dissociates, and GTP binds. (nucleotide exchange)
  4. The alpha subunit-GTP complex dissociates from the beta-gamma complex. Both are active and can go on to activate an effector protein.
25
Q

The ______ is a parasympathetic GPCR that binds ACh and opens _____ channels. What effect does this have on the heart?

A

muscarinic acetylcholine receptor, K+, hyperpolarizes cardiac muscle sarcolemma, thereby reducing heart rate

26
Q

What effect do cholera and pertussis toxins have on GPCRs?

A

Cholera: modifies Gs-alpha subunit and prevents GTP hydrolysis -> stuck “on,” causing excess cAMP
Pertussis: modifies Gi-alpha subunit and prevents dissociation of ADP -> stuck “off,” causing excess cAMP (turning off an inhibitory pathway)

27
Q

The Gs and Gi classes of G-alpha proteins use ____ as an effector and ___ as a second messenger. The Gq class uses ___ as an effector and ____ as second messengers.

A

Adenylyl cyclase; cAMP -> PKA

Phospholipase C; IP3/DAG -> PKC

28
Q

What are some examples of Gs-α type receptors?

A

β-adrenergic, glucagon, serotonin, vasopressin

29
Q

What do GLP1 agonists do?

A

They are drugs that mimic glucagon-like peptide 1 (GLP1) and increase its effect (agonists). Like GLP1, GLP1 agonists PROMOTE INSULIN secretion and INHIBIT GLUCAGON secretion, making it a useful drug for DM2 patients.

It also decreases appetite and induces early satiety, leading to weight loss.

30
Q

What are some examples of Gi-α type receptors? Which receptor activates the beta-gamma complex so it can open K+ channels?

A

α1-Adrenergic receptor, muscarinic ACh receptor leads to K+ channel opening and decrease in heart rate (hyperpolarization)

31
Q

In which Gα class is the α2-Adrenergic receptor?

A

Gq-α

32
Q

How does the IP3/DAG pathway increase [Ca2+] in the cytosol?

A
  1. Ligand binds GPCR, activates Gq-α, which activates phospholipase C
  2. Phospholipase C cleaves PIP2 into IP3 + DAG
  3. IP3 opens ER Ca2+ channels, increasing [Ca2+] in cytosol
  4. High [Ca2+] sends cytosolic PKC to plasma membrane, where it is activated by DAG. (PKC then phosphorylates downstream enzymes)
  5. As ER Ca2+ stores are depleted, a protein associated with the IP3-gated Ca2+ channels binds to and opens Ca2+ channels in the plasma membrane. Now Ca2+ enters from extracellular space.
33
Q

How is CaM kinase II activated?

A

CaM kinase II (Ca-calmodulin-dependent protein kinase II) is activated by calmodulin, which is only in its catalytic state when bound to calcium. Ca-calmodulin activates CaM kinase II, which then autophosphorylates to become “fully active.” Even after dissociation of ca-calmodulin, CaM kinase II remains “partially active” (~80%) so long as it’s phosphorylated. This may be instrumental in memory processes in the brain.

34
Q

Describe the ACh/IP3/NO pathway in the alleviation of angina.

A
  1. ACh binds its GPCR -> Phospholipase C -> IP3 -> Ca/Calmodulin -> NO synthase (produces nitric oxide, NO)
  2. NO -> guanylyl cyclase -> cGMP -> PKG -> pathway resulting in smooth muscle relaxation and vasodilation
35
Q

Cardiac hypertrophy is an adaptive response to many cardiac diseases (HTN, MI, arrhythmias, etc). What role do Ca2+ and calcineurin play in cardiac hypertrophy and what drugs can be used?

A

Mutations in sarcomeric proteins –> increase [Ca2+] (an adaptive response, for better contractility/cardiac output).
Ca-calmodulin and SUSTAINED increase in [Ca2+] –> activation of calcineurin.
Calcineurin activates NFAT.
NFAT –> nucleus, affects immune response and cardiomyocyte HYPERTROPHY.

Calcineurin is inhibited by cyclosporin A (CsA) and FK506.
Thus, CsA and FK506 are anti-cardiac hypertrophics, immunosuppressants.

36
Q

‘Homologous desensitization’ is when active GPCRs activate ____, which phosphorylate the GPCRs. Receptor phosphorylation induces the recruitment of _____, leading to ____.

A

GPCR kinases (GRKs), β-Arrestin, receptor endocytosis

37
Q

What type of receptor is utilized in growth factor signal transduction? What broad class of cell surface receptor are these?

A

receptor tyrosine kinases, enzyme-linked receptors

38
Q

What is the first thing to happen as a result of ligand binding to RTKs?

A

The RTK homodimerizes and autophosphorylates its cytoplasmic tyrosine residues.

39
Q

Give some important examples of RTKs.

A

epidermal growth factor (EGF) receptors, PDGF receptors, insulin receptor

40
Q

How many signaling proteins can bind simultaneously to one activated RTK (to the phosphotyrosines)?

A

Many

41
Q

GRB2 is an RTK adaptor protein. It has a domain called ____ that complexes with ___. The two of them (GRB2 and ___) mediate the interaction between the RTK and ____.

A

Src homology domain (SH2, SH3), Sos, Sos, Ras

42
Q

What is the GEF that promotes dissociation of GDP from Ras? Is the resulting GTP-Ras active or inactive? What do Ras and other members of the Ras superfamily do?

A

Sos; active; activates downstream targets in pathways regulating cell growth, differentiation and migration

43
Q

Constitutive activation of Ras (and other Ras family GTPases) occurs when mutations render Ras incapable of hydrolyzing GTP. This is present in 20-30% of ______.

A

human cancers

44
Q

Ras GTPases have evolved to be catalytically slow in order for their signals to last longer. What proteins accelerate GTP hydrolysis in Ras?

A

GTPase-activating proteins (GAPs): rate changes from .02/min -> 2000/min
Regulators of G-protein signaling (RGS), a GAP homolog that binds with Gα: rate changes from 3/min to 300/min

45
Q

What proteins are activated following Ras activation?

A

Ras -> Raf -> Mek -> Erk
aka…
Ras -> MAP kinase kinase kinase -> MAP kinase kinase -> MAP kinase

MAP kinase is a S/T kinase that can translocate into the nucleus and activate many proteins and transcription factors that promote cell growth and differentiation.

46
Q

Neuro-cardio-facial-cutaneous (NCFC) syndromes are caused by _____. What else is caused by this?

A

germline mutations in the Ras pathway; Noonan syndrome, Costello syndrome

47
Q

What is PI(3)K and how is it regulated?

A

A lipid kinase involved in proliferation, differentiation, and cell survival (INHIBITS APOPTOSIS). It is activated by Ras-GTP and by the binding of its SH2-containing regulatory subunit (e.g.p85a) to activated RTKs. Active PI(3)K activates PKB, which inhibits apoptosis.

Ras-GTP + active RTKs ==> PI(3)K ==> PKB ==> inhibit apoptosis

PI(3)K is inhibited by PTEN. Loss of function of PTEN causes cancer. Thus, regulation of PI(3)K function is critical for normal cell growth and differentiation.

48
Q

____ are a family of mediators of cell-to-cell communication that are required for immunity, hematopoiesis, inflammation, and neural and embryonic development. They are activated by ______.

A

cytokines, nonreceptor protein tyrosine kinases (PTKs)

49
Q

Insulin receptor is a ___ that phosphorylates ___, leading to the metabolic effects of insulin.

A

RTK, IRS (insulin receptor substrates)

Biochemistry (12 decks)

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