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Endo/Repro Midterm > Hormone Signaling Pathways > Flashcards

Hormone Signaling Pathways Flashcards

1
Q

Activation of hormones involves binding to a ____ on cells and activating _______ and/or alteration in gene expression that lead to a response.

A

Receptor

Signal transduction

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2
Q

Nine steps of hormone signaling

A 
Biosynthesis
Storage
Secretion
Transport to target tissue/cells
Recognition and binding to receptors
Activation of signal transduction
Amplification and relay of signal
Cellular response
Degradation
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3
Q

Stimulus -> hormone released from signaling cell -> signaling molecules travel to their target cell (through blood, etc.) -> ____ signals can easily enter membrane of target cell (can use a receptor) -> begins a cellular response

A

Hydrophobic

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4
Q

Signaling molecule released by a cell distant from target cell and transported via bloodstream to target cell

A

Endocrine signaling

Ex: epinephrine

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5
Q

Signaling molecule released by one cell type and diffuses to a neighboring target cell (locally) of a different cell type

A

Paracrine signaling

Ex: testosterone

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6
Q

Signaling molecule acts on the same cell type as the secreting cell

A

Autocrine signaling

Ex: Interleukin 1

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7
Q

Signaling molecule stays attached to the secreting cell and binds to a receptor on an adjacent target cell (forms bridge)

A

Juxtacrine signaling

Ex: heparin

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8
Q

What are hydrophilic hormones?

Do they use a second messenger?

Examples?

Receptors?

A

Can not penetrate the plasma membrane so interact with specific receptors at the cell surface

Yes, the receptor complex initiates production of a second messenger inside the cell that triggers a cellular response (cAMP, Ca, IP3)

NE, E, insulin, glucagon, histamine, serotonin, melatonin, dopamine, ACh, cytokines, TSH

G protein-coupled receptors, receptor tyrosine kinases

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9
Q

What are lipophilic hormones?

Do they use a second messenger?

Examples?

Receptors?

A

Pass through plasma membrane

No, the hormone binds to specific receptor proteins inside the cell; molecule receptor complex acts as a transcription factor

Progesterone, estradiol, testosterone, cortisol, aldosterone, vitamin D, thyroxine, retinol, retinoic acid

Cytoplasmic receptors, nuclear receptors

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10
Q

_____ receptors exist in an inactive complex with the HSP 90; HSP dissociates; the hormone-receptor complex translocates to the nucleus where it binds to a DNA sequence called ______ in the promoter region of specific genes.

A

Cytoplasmic receptors

Hormone response element (HRE)

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11
Q

This receptor is already present in the nucleus and bound to DNA; the hormone signal activates the complex.

A

Nuclear receptor

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12
Q

Hydrophilic medications have a ____ half life.

Example?

Lipophilic medications have a _____ half life.

Example?

A

Short

Epinephrine; used to treat severe acute allergic rx

Long

Oral contraceptives

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13
Q

How are G protein coupled receptors activated and inactivated? (GPCR)

What role do GEF and GAP play?

A

G protein with three subunits

Inactive G protein exchanges GDP for GTP through the action of the guanine nucleotide exchange factor (GEF)

Active GTP alpha subunit separates from beta and gamma to do the work

To return to inactive, intrinsic GTPase activity of G protein hydrolyzes GTP to GDP and Pi; accelerated by GTPase-activating protein (GAP)

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14
Q

Fx GPCR signaling variations:

Gs?

Gi?

Gt?

Gq?

A

Stimulates adenylate cyclase, forms cAMP, PKA, phosphorylates targets (epinephrine with beta adrenergic receptor, histamine)

Inhibits adenylate cyclase (E and NE with alpha receptor, dopamine)

Stimulates hydrolysis of cGMP by phosphodiesterase

Works through phospholipase C, IP3, activation of PKC (ACh)

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15
Q

What is receptor tyrosine kinase? (RTK)

How does it work?

How is it terminated?

A

Extracellular domain that binds to a ligand

RTK binds to a ligand (hydrophilic hormone) causing dimerization; dimerized receptor then phosphorylates tyrosine residues; phosphotyrosines are recognized by adaptor and docking proteins; this activates downstream signaling pathways (RAS dependent/independent); this triggers phosphorylation of specific protein targets that alter gene expression

Degradation of ligand, RAS inactivation, dephosphorylation, ligand-induced endocytosis of receptor

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16
Q

Insulin synthesis and secretion:

____ upregulates preproinsulin mRNA

Translated into ____ and translocated to ____ lumen

Cleaved by ____ to form proinsulin

Folded and transported to _____.

Packaged into immature ______ then cleaved by ____ to form insulin and C peptide

Immature granules become _____ that contain hermetic crystalized _____.

____ and ____ are released together.

A

Glucose

Preproinsulin; ER

Protease

Golgi

Granules; proteases

Mature granules; insulin

Insulin and C peptide

17
Q

____ stimulates the release of insulin in two phases, what are they?

Where does each release get their insulin granules?

A

Glucose

First and second

First: limited pool of granules called readily releasable pool (RRP)

Second: larger pool called reserve pool

18
Q

Glucose in blood -> enters pancreatic ___ cells though ___ transporter -> glucokinase phosphorylates glucose -> glycolysis -> TCA cycle -> make ATP -> ___ levels of ATP close K+ channel -> causes ____ of membrane -> opens Ca channel -> helps release insulin granules from pancreatic beta cells

A

Beta

GLUT 2

High

Depolarization

19
Q

What type of signaling does insulin use?

A

Receptor tyrosine kinase

20
Q

Describe insulin signaling through the RAS-dependent RTK pathway

A

Insulin binds to dimerized insulin receptor -> phosphorylation of insulin receptor -> recruits insulin receptor substrate (IRS-1) -> IRS-1 is phosphorylated and binds to adaptor protein GRB-2 -> activates RAS and MAPK pathway -> phosphorylation of proteins -> alters gene expression of glucokinase -> stimulate glycolysis and glycogen synthesis -> lowers blood sugar

21
Q

Describe insulin signaling through the RAS-independent RTK pathway

A

Insulin binds to dimerized insulin receptor -> phosphorylation of insulin receptor -> recruits insulin receptor substrate (IRS-1) -> IRS-1 is phosphorylated and recruits enzyme PI3-kinase -> activates PKB -> phosphorylates proteins causing translocation of GLUT 4 (transporter in muscle and adipocytes) -> GLUT 4 moves from cytoplasm to plasma membrane -> influx of glucose and increase glycogen synthesis

22
Q

Reduced sensitivity to insulin (normal amount of insulin doesn’t cause the expected response)

A

Insulin resistance

23
Q

What causes insulin resistance?

A

Defects in insulin signaling (receptor activation to translocation of GLUT 4 transporters in adipose and muscle tissue)

Mutations in insulin receptor

Defect in insulin binding domain on extracellular side

Variations in intracellular domain

24
Q

Insulin resistance can be caused from increased phosphorylation of a ____ domain by ____ kinase instead of tyrosine in the insulin receptor.

This inhibits formation of ____ which prevents both RAS pathways.

____ kinase is activated by cytokines, free fatty acids, DAG, ceramide, inflammatory molecules.

A

Serine

Ser/Thr kinase

IRS

Ser/Thr kinase

25
Q

This hormone stimulates gluconeogenesis

A

Cortisol

26
Q

These hormones stimulate glycogen breakdown

A

Epinephrine, glucagon

27
Q

This hormone promotes glycogen synthesis, glycolysis, inhibiting gluconeogenesis

A

Insulin

28
Q

Type of receptors that bind to lipophilic hormone ligands

Example of these lipophilic hormones

A

Classic nuclear receptor

Glucocorticoids, mineralocorticoids, estrogen, progesterone, androgens

29
Q

Receptors discovered by DNA sequencing that bind to lipophilic hormone ligands

Examples?

A

Orphan receptors (part of nuclear receptor superfamily)

Adopted orphan receptors: retinoids, thyroid hormones, vitamin D, xenobiotics, androstane

30
Q

Nuclear receptors can localize in the ____ or _____.

After ligand binding, they ____ to the nucleus and influence ____.

Disease involved in dysfunctional NR signaling?

A

Nucleus or cytosol

Translocate; gene expression

Diabetes, cancer, reproductive disorders, inflammation, CHF, obesity

31
Q

Describe the structure of a nuclear receptor, domains and inactive and active form

A

Three binding domains: activation function, DNA binding, ligand binding

Inactive form: ligand binding domain surrounded by inhibitory proteins

Active form: conformational change allows activator proteins to surround the ligand binding domain; DNA binding domain now binds to regulatory sequence on DNA (hormone response element, HRE)

32
Q

Two steps of steroid hormone mechanism

A

Steroid hormone binds to receptor and causes a response (primary response); this initiatives the secondary response

33
Q

Estrogen receptor (ER) uses a ____ transcription factor

What are the two types?

A

Estrogen dependent

ER alpha, ER beta

34
Q

Receptor present in the female reproductive tract including the uterus, vagina, ovaries, mammary gland, hypothalamus, endothelial cells, vascular smooth m

Predominant in growth regulation like in types of breast cancers

A

Estrogen receptor alpha

35
Q

Receptor present in the prostate, ovaries, lungs, brain, bone, vasculature

A

Estrogen receptor beta

36
Q

ER is a ____ receptor.

How does the ER work?

A

Nuclear

Hormone (estrogen) binds to ER -> dimerizes ER -> activator proteins recruited to the receptor -> activates general transcription apparatus (GTA) -> increases activity of histone acetyl transferase (HAT) -> loosens the chromatin structure -> allows GTA to bind to DNA and up-regulate transcription

37
Q

Antagonist of estrogen used to treat breast cancer

How does it work?

A

Tamoxifen

Metabolized by cytochrome P450 into active form of 4-hydroxy-tamoxifen -> binds to ER -> attracts difference proteins -> leads to activation of histone deacetylase (HDAC) -> keeps chromatin tight -> prevents GTA from binding to DNA -> inhibit transcription

Endo/Repro Midterm (11 decks)

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