Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/27

Click to flip

27 Cards in this Set

  • Front
  • Back
Transmembrane signalling
ligand --> receptor --> transducer --> 2nd messenger --> target -->effect

2nd messanger can be:
- extruded
- sequestered
- degraded
Glycogenolysis

Epinephrine
- inc activity of phosphorylase: catalyze glycogen --> G1P
-inc activity bc inc in -/+ AMP ration --> conversion of phosporylase from dependent AMP, phosphorylase b to independent from AMP, phosphorylase a (a is active form)

--> reversible covalent modification --> phosphorylation, regulate enzyme activity
Glycogen synthase
- enzyme that catalyze syn of glycogen
- can be phosphorylated at mult sites with complex result on allosteric regulation of enzyme activity
Changes in allosteric regulation of an enzyme
are used to study regulation by covalent modifications

- advances in methods that determine protein structure (mass sepc) will likely inc the use of structural measurements and dec the use of functional measurements
cyclic AMP
- synthesized from ATP by adenylate cyclase
G protein
- regulates adenylate cyclase by G protein cycle
-binding of GTP to G protein produce effect
- hydrolysis of GTP to GDP terminates effects and the release of GDP
Lock G protein into active state or inactive state
- hydrolysis resistant analogs of GTP can lock a G protein into its active state.

-Analogs of GDP can lock a G protein into the inactive state

- problem: for drugs lack of specificity
GAP
GTPase activating protein, some systems req for expression of GTPase activity for adenylate cyclas --> GAP resides iwthing Galpha
Gs
1. stimulate adenylate cyclase
- promote release of GDP from alpha subunit of Gs, bind with GTP, dissociation of alpha
- hydrolysis of GTP stops syn of cAMP
- hormones that stimulate adenylate cyclase activity also stimulate a GTPase activity
- turnover rate GTP slow 1 per min
Gi
inhibit adenylate cyclase activity
-promote release of GDP from alpha subunit of Gi , bind GTP , dissociation ofr Beta gamma, Gi alpha -GTP inhbits adenylate cyclase catalytic subunit
cAMP- dependent protein kinase

aka protein kinase A, PKA
- binding cAMP, regulatory subunits release catalytic subunits --> phosphorylates several susbtrates
phosphorylase kinase
- calmodulin kinase, regulated by Ca binding to a subunit of the enzymes termed calmodulin
Phosphatase
catalzye dephosphorylation of proteins --> reversing effects of phosphorylation
1. cascade of phosphorylation

2. cAMP frequency

3. Phosphorylation
1. allows amplification

2. causes a coordinated inc in a differentiated function of a cell, which freq inc energy consumption and catabolic processes. In the endocrine system this func is freq the secretion of a hormone

3. can alter allosteric regulation (inhbiotry and activating) of an enzyme) but also apparent Km of an enzyme
Homologous desensitization
receptor phosphorylation and internalization
Heterologous desensitization
mediated by cAMP
1. inc rate in degradation of cAMP by enzyme phosphodiesterase (PDE)
2. inc rate of extrusion of cAMP from cell by active pumping or facilitated diffusion
3. dec in effective activity of cAMP- dependent protein kinase
- free catalytic subunit of cAMP dependent protein kinase has shorter intracellular half life than subunit associated with the R subunit
4. generation of inhbitors of PKA
Bacterial toxins: mono- ADP- ribosyltransferases
bacterial toxins catalyze the mono-ADP-ribosylation of the G protein alpha subunits. The rxn transfers the ADP ribose moiety of NAD to the target protein
Cholera toxin
- vibrio cholerae--> responsible for sudden life thretening voluminous diarrhea of the disease cholear
- act by ADP ribosylating G salpha, dramatically retards the hydrolysis of GTP
- persistent activation of adenylate cyclase
Pertussis toxin
- toxin produced by bordetella pertussis
- cause of the disease pertussis or whooping cough
- pertussis toxin ADP - ribosylates G i alpha which retards the dissociation of GDP from Gi alpha prevents G i alpha from bindng GTP and blocks hormone inhbition of adenylate cyclase
- hormones that stimulate adenylate cyclase --> more potent, their normal effects are exaggerated
Both cholera and pertussis toxins block the GTPase activity of a G protein
Recombinant analogs of these toxiins lacking ADP- ribosyltransferase activity are now included as antigens in vaccines to protect against disease
Tumors
ACtivating mutations in G proteins can cause tumors via the persistent signal to perform the cells' differentiated function which leads to cell division
GHRH (growth hormone releasing hormone)
acts via cAMP to promote synthesis and release of GH from pituitary cells and promotes proliferation of cultured pituitary cells.
Drugs
- influence cAMP metabolism
- mimic hormones that stimulate adenylate cyclase
- competative inhbitors of hormones
Histamine
ex. histamine- block histamine stimulation of acid secretion in the stomach
Beta blockers
ex. beta blockers -- prevent epinephrine from activating adenylate cyclase spares the heart
Isoproterenol
ex. isoproterenol inc cAMP dec smooth muscle tension in the lung during asthmatic attack
Methyl xanthine derivatives (caffeine)
inhibitors of cAMP phosphodiesterase (PDE)
- some compounds act as adenosine analogs at adenosine receptors which inhbit adenylate cyclase rather than by inhbiting PDE