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Cell Biology (311) > Receptors > Flashcards

Receptors Flashcards

Exam 2

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1
Q

What are receptors?

A
  • proteins that interact with a ligand(s) that result in a change in cell behavior
  • short term: in cytoplasm
  • long term: genomic activation (steroids only have long term)
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2
Q

What is a ligand?

A
  • a molecule (naturally occurring or synthetic analog) that stimulates a receptor
  • Three possibilies of this action
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3
Q

What are the three possibilities of ligands binding to receptors?

A
  • agonist- activates the receptor
  • antagonist- blocks/inhibits receptor activity
  • modulator- regulates/influences the effect of the receptor
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4
Q

Hydrophobic v hydrophilic ligands

A
  • hydrophobic- pass through the membrane (ex. steroid hormone)
  • Hydrophilic cannot pass through the membrane (many examples)
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5
Q

Receptors sorted by distance traveled of ligand

A
  • Plasma membrane attached proteins- angstroms (receptors and ligands are on membranes of touching cells-bound to each other)
  • Synaptic- nanometers (neurochemical)
  • Autocrine- micrometers
  • paracrine (cell to cell, cell releases ligand and it interacts w another)- micrometer
  • endocrine- can be up to meters
  • phermones- person to person
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6
Q

Autocrine signaling

A
  • Target cell is the one that synthesizes the ligand.
  • Ex. some cancer cells produce their own mitogen (ligand that triggers cell division)
  • Experiements: start w 2 cells, wait 5 days, now have 4. Start with 10 cells, wait for 5 days, now have 100. Due to autocrine signaling of growth factors. Normal cells require autocrine factors in cell culture.
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7
Q

(According to slides) receptor activation and signal transduction result in:

A
  1. changes in enzyme activity
  2. protein abundance
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8
Q

Types of signaling w membrane insoluble ligands

A
  1. Ligand gated ion channels- no pumps, just flows down concentration gradient (nAch rec. once bound to Ach passes na+ and k+, fastest)
  2. receptor mediated endocytosis (cell absorb molecule), takes 60-90 mins (slowest)
  3. receptor associated kinases (cytokine receptors and receptor tyrosine kinases)
  4. GDCRs
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9
Q

Steroid and their receptors overview

A
  • hydrophobic
  • receptors typically not on cell membrane, most are soluble in the cytoplasm
  • vitamin-D, estradiol, testosterone, cortisol
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10
Q

steroid receptor

A
  • Structure (2 domains): hormone binding (binds to steroid hormones) and transcription activated (interacts w genome to regulate gene expression).
  • In inactive state, the receptor is part of an inhibitory complex that includes heat shock proteins (hsp/hsp90) which prevent receptor from functioning.
  • Activation: when hormon binds confomation change occurs, allowing receptor to translocate to the nucleus
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11
Q

Steroid receptor responses

A
  1. Primary response: Activated receptor can initially disable its own production and enable prodction of proteins involved in the secondary response.
  2. Secondary response: Long-lasting effects on gene expression and cellular function
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12
Q

Steroid signaling clinical relevance

A
  • Patients hospitalized w COVID-19 who were vitamin D deficient experienced worse outcomes than ppl w normal vitamin d levels (below 20ng/mL)
  • nearly double risk of testing positive for covid
  • Vit D may turn down the “cytokine storm” through immune regulation

low lvls also associated w increased risk for respiratory infection in general

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13
Q

Vitamin D

A
  • Helps the body absorb calcium
  • helps immune, muscle, and nervous system function properly
  • may play a role in controlling normal breast cell growth and may be able to stop breast cancer cells from growing. may be similar relationship w colon cancer and other non-skin cancers as well
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14
Q

types of endocytosis

Phagocytosis vs pinocytosis vs receptor mediated endocytosis

A
  • Phagocytosis: engulfs food
  • pinocytosis: engulfs extracellular fluid
  • Receptor mediated: uses receptors to selectively uptake molecules that bind to the receptor.
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15
Q

What is internalized into the cell during receptor mediated endocytosis?

A
  • the ligand and the receptors
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16
Q

RME example

Ferrotransferrin

A
  • Delivers iron into cells.
    1. Receptor binds to ligand.
    1. Formation of a coated (clathrin) pit
    1. Early Endosome: membrane protein pump pumps ions into endosome
    1. Late endosome. Low pH (5) causes release of Fe3+ from ligand. The ligand remains bound to the receptor
    1. Apotransferring (no iron) goes to cell membrane and is released (recycled). pH is neutral now

transferrin is blood plasma glycoprotein

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17
Q

What is clathrin?

A
  • Coats vesicle in endocytosis
  • Self assembles w little to no ATP. Triskleion.
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18
Q

What is dynamin?

A
  • Pinches off the coated pit to form a coated vesicle. We can manipulate its function
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19
Q

Why do you see significant increase in the number of coated pits on the cell surface when temperature is decreased?

A

Because the low temp slows endocytosis causing the coated pite to accumulate without begin internalized into the cell

20
Q

How can we determine if the change in pH from 7.0 to 5.0 is required for offloading cargo in the late endosome?

A
  1. Incubat the cells in dilute ammonium chloride.
  2. Add bofilomycin to the culture (it can selectively inhibit the proton pump in the late endosome)
  3. Use chloroquine which selectively accumulates in the lysosome, increasing it pH to 7.0
21
Q

Many viruses infect cells via…

A

rceptor mediated endocytosis

22
Q

Chloroquine

A
  • selectively acumulates in the lysosome, increasing its pH
  • used to treat malaria and suggested by Trump as a means to address covid
23
Q

Example of RME

LDL RME: LDL particle

A
  • Cholesterol center (apolar)
  • Phospholipids with polar surface
  • Apolipoprotein D (protein to which the LDL receptor binds)

Complex molecular structure package

low density lipoprotein

24
Q

LDL pulse chase experiment

A
  • can monitor movement and fate of LDL particles within cells by expoing them to a short pulse of radiolabeled LDl, followed by chase period where unlabeled LDL is added to track how the labeled LDL is processed and transported within the cell overtime
  • allows researchers to monitor uptake, intracellular trafficking, and degradatio of LDL particles within a cell culture
25
Q

LDL steps

similar to ferrotransferrin

A
  1. LDL particle brought into lysosome
  2. Broken down in late endosome into components (amino acids, cholestoerl, fatty acids)
  3. pH 5 LDL particle released bc B-propeller becomes protonated and binds to the ligand binding arm
  4. at neutral pH ligand-binding arm free to bind to another LDL particle
26
Q

Familial hypercholesterolemia

A
  • Excessively high lvls of LDL, so high that LDL particles precipitate out into skin/blood vessels
  • not easily treated with statins
27
Q

Molecular basis of FH

A
  • LDL receptor is not synthesized enough. Note that while the LDL-Rs recycle some are lost so there is a measurable synthesis rate
  • LDL-R are not properly transported from the RER to the plasma membrane
  • LDL-R doesn’t bind LDL properly due to a defect in ApoB
  • LDL-R don’t cluster properly in the coated pit due to defects in the NPXY domain
  • LDL-R dont recycle properly
28
Q

LDL receptor as therapeutic target for Alzheimer’s disease

A
  • Observation: high concentrations of LDL receptors in the brain protect mice from Alzheimer’s disease
  • How did they do the study?: Crossed a transgenic Alzheimer’s mouse with a high LDL brain receptor mouse. The progeny still developed Alzheimer’s but much less so due to less “tau” protein generated in the neurons
29
Q

“Scientists create high cholesterol mouse, cure it with gene therapy- a possible approach to treating FH”

A
  • Mouse created at Baylor is not transgenic but rather is a human familial hypercholesterolemia xenograft mouse model
  • Mouse chimeric liver is 95% humanized through transplant of LDL diseased human cells (loss of function mutations in LDLR) from liver transplant operation
  • Mouse was “cured” through single dose transfection of human wild type LDLR
30
Q

GPCRs fast facts (G protein coupled receptors)

A
  • Most numerous of the receptors
  • 800+ functional GPCRs which constitute about 4 percent of all idenfified human proteins
  • Some are “orphan receptors”- no known ligand
  • 35% of all drugs work through the GPCRs
  • 134 GPCRs are targets of drugs (beta 2 adrenergic receptor is target of many asthma inhalers)
31
Q

General mechanism of G protein coupled receptors (serpentine receptors)

A
  • Once activated by ligand, the receptor binds to a partner G protein and promotes exchange of GTP for GDP, leading to dissociation of the G protein into a and By subunits that mediate downstream signals
32
Q

Three types of G protein

A
  • Class A: Trimeric (serpentine bc 7 [ass membrane proteins, rhodopsin like)
  • Class B: monomeric (Ras)
  • Class C: biggest
33
Q

How do you study receptors such as GPCRs?

A
  • X ray crystallography can be used that involves analyzing the diffraction patterns coupled to analytical programs to deduce structure
  • Radioligand binding assays can reveal competitive agonists or antagonists- most important
  • Measuring the effect of GPCR stimulation by analyzing activity of effector enzyme
  • Nanodisks put the receptor in the bilayer
34
Q

Competitive binding assays to measure receptor function

A
  • Receptor and natural ligand bind together and can be characterized
  • Do the same but also have unknown ligands. See if the known ligand is displaced.
  • Lets you know which has higher affinity to the receptor
35
Q

Nanodisk

A
  • synthetic model membrane system that places receptors in their native environment
  • MSP (membrane scaffold protein) serves as a belt that wraps around the membrane system
36
Q

GTPase switch proteins

A
  • can be turned on and off like protein kinases activating target proteins
  • can be regulated by guanine nucleotide exchange factor (GEF) and GAP (GTPase activating protein)

GEF swaps GDP to GTP, GAP does opposite

37
Q

Muscarinic vs nicotinic Ach receptor

A
  • nic is ligand gated
  • musc is GPCR
38
Q

Muscarinic Ach Receptor

A
  • ex. of GPCR
  • found in heart
  • K+ channel opens, slows heart rate and heart contraction rate
  • FRET helps analyze the G protein cascade bc see conformation changes in GPCRs (energy transfer)
39
Q

Visual transduction system overview

A
  • ex. of GPCRs
  • one of the most complicated systems to figure out
  • rhodopsin
  • Rod has inner and outer segment (all activity in outer segment)
  • cell responds to light, translates light into neurotransmitters
40
Q

Visual transduction system

Retinal pigment epithelium 3 roles

A
  • Phagocytose shed outer segment disks
  • absorb stray photons to avoid back scatter
  • provides glucose to the rod outer segment (this system uses a lot of energy- GLU-1 brings ATP)
41
Q

Challenges studying visual transduction system

A
  • Rod photoreceptors are very slender making single cell electrophys hard
  • Have to look at presence of light or dark for electrophys- had to do it in the dark for this (and in situ)
  • Change in membrane potential was not conventional
42
Q

Change in membrane potential was not conventional meaning (For study of visual transduction system)

A
  • Conventional: typical action potential. neuron stimulated/depolarization as normal (start at -70 mV, go up to +55)
  • Rod photoreceptor: not conventional- starts at -30, goes to -70 (hyperpolarization)
43
Q

Vision is a G protein process explained

A
  • Begins w rhodopsin. Light interacts, and now rhodopsin is light activated.
  • Dissociation event. Then binds to effector protein (PDE= effoectorprotein. cGMP phosphodiesterase)
  • Target is cGMP (cGMP phosophodiesterase), converted to GMP.

open cGMP gated ion channel has high cGMP (this depolarizes membrane and more NT released, closed has low cGMP)

44
Q

cGMP phosphodiesterase

A
  • Tetramer- inactive
  • Y subunits are inhibitors. Dimer- active
  • Causes cGMP to become GMP. cGMP is an active form that keeps channels open. GMP is inactive form, leads to less cGMP so channels close
45
Q

Summary of visual transduction

A
  • in the dark there is high cGMP- proton channels (Na and Ca) open
  • In the light there is low cGMP- proton channels close. Why it hyperpolarizes.
46
Q

Why does it take awhile for eyes to adjust to different amounts of light?

A
  1. Rhodopsin kinase: when light hits rhodopsin, it conformationally changes and activates. Rhodopkin kinase phosphorylates activated rhodopsin. This reduces the activity of rhodopsin, preventing prolonged activation in bright light conditions.
  2. Transducin: g protein activated when rhodopsin is stimulated by light. When activated, exchanges GDP for GTP, leading to activation of PDE which reduces cGMP levels (which closes ion channels leading to hyperpolarization)
  3. Arrestin: binds to phosphyrlated rhodoopsin which further prevents transducin activation. helps to desesitize the photoreceptor to ensure it does not continue responding to light when it is already activated

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Cell Biology (311) (8 decks)

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