signaling 1&2 Flashcards

19.07.26

1
Q

why is a cell important in medicine?

  1. think balance
  2. what happens when regular functions are compromised
  3. target for what?
A
  1. signaling controls every aspects of homeostasis in the human body
  2. defective or uncontrolable signaling pathways can lead to developmental abnormalities or seriour diseases
  3. signaling pathways are major pharmacological targets
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2
Q

what are the major cell responses to signals?

  1. multiply
  2. relocate
  3. types
  4. energy change
  5. your not wanted
A
  1. cell proliferation
    1. clonal expansion of specific B and T cells after encountering a foreign antigen
  2. cell development
    1. chemokines induce immune cell migration to inflammatory sites
  3. cell differentiation
    1. embryonic development
    2. organogenesis
    3. hematopoiesis
  4. alter metabolic and/or secretory activity of the cell (most general)
    1. tissue repair post trauma
    2. histamine release by mast cells during an allergic response
    3. insulin stimulates glucose uptake, glycogen and lipid synthesis
  5. cell death (apoptosis)
    1. shrinking of mammary glands after lactation period
    2. removal of the web between the fingers/toes during embryonic development
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3
Q

there are three types of signaling abnormalities commonly seen what categories do the following fall into

  • overproduction of signaling molecules
  • certain femal infertilities(lack of gonadotropins)
  • deficient signal detection (receptor)
  • Type 1 diabetes mellitus (lack of insulin
  • interference from other signaling pathways
  • lack of signaling regulation
  • hypothyroidism
  • deficient intracellular signaling pathways
  • hyperthyroidisn
  • cAMP overproduction in cholera or whooping cough
  • type two diabetes mellitus
A

signaling abnormalities

  1. lack of chemical signals
    1. certain female infertilities (lack of gonadotropin)
    2. type 1 diabetes mellitus (lack of insulin)
    3. hypothyroidism (reduce thyroid hormone levels)
  2. insensititivity to signaling molecules ( cells do not respond as they should)
    1. deficient signal detection(receptor)
    2. deficient intracellular signaling pathway
    3. interference fromr othe signaling pathways
    4. type 2 DM
  3. hyper-reactivity to signals
    1. overproduction of signaling molecules
    2. lack of signaling regulation
    3. hyperthyroidism
    4. cAMP overproduction in cholera or whooping cough
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4
Q

explain the signal difference between normal/tumor cell

A
  1. general
    1. proliferation
    2. migration
    3. differentiation
    4. metabolic change
    5. death
  2. tumor
    1. uncontrolled cell proliferation
    2. decreased cell death
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5
Q

define the four types of signaling

A
  1. contact mediated-signaling though cell-cell contact
    1. examples
      1. antigen presenting cells,
      2. communication between muscles
  2. paracrine signaling- short distance signaling between different cells
    1. examples
      1. action of ACh at neuromuscular junction
      2. cytokines
  3. autocrine signaling- short distance signaling involving the same (or same type of ) cell(s)
    1. examples
      1. prostaglandins
  4. endocrine signaling - long distance signaling between endocrine glands and target cells
    1. hormones
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6
Q

describe the type of signaling in this photo and give two examples

A

contact mediated

  1. antigen presentation
  2. gap junctions in muscle cells
    1. allowing secondary messengers to tranverse cells
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7
Q

describe the signaling type in the photo give details about the 3 mediums of this type of signaling

A

paracrine signaling: cytokines

  1. chemcial signaling
    1. low concentration
    2. short half life
  2. neurtransmitter
    1. high concentration
    2. very short half life
  3. receptors
    1. high/low affinity
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8
Q

describe the type of signaling in this photo

give reasoning behind the two modalities of this group

A

autocrine signaling:prostaglandins

  1. chemical signaling
    1. low conecntration
    2. short half-life
  2. receptor
    1. high affinity
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9
Q

describe this type of signaling explaing the following

  1. source
  2. half life
  3. target
  4. function
A

endocrine signaling

  1. source
    1. endocrine glands
  2. half life
    1. long half life (min-hr-days)
  3. target
    1. recognized by specific, high affinity receptors
    2. often attached to peptide to assist its travel
  4. function
    1. cause relatively slow cell responses
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10
Q

Define this type of junction, terms in blanks and give examples of the following

  1. chemical signals
  2. signal detection (receptors)
  3. conversion of signal
  4. regulation
A

this is an example of the essential signaling steps in a neuromuscular junction

  1. chemical signal
    1. ACh
  2. receptors
    1. nicotinic ACh
      1. skeletal muscle,
      2. Na/K channel
    2. muscarinic ACh
      1. heart muscle
      2. G-protein linked
    3. conversion of signal
      1. nicotinic ACh
        1. lets Na in and K out
      2. muscarininc ACh
        1. regulates K
    4. regulation
      1. ACh esterase
        1. degrades excess ACh

difference in reaction to ACh,

  1. SM-increase contraction
  2. heart-decrease contraction
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11
Q

look at the neuromuscular junction and think about the types of diseases associated with a fluction in ACh signaling

  1. too little signal
  2. too much signal
    1. how does this effect the heart vs skeletal muscle?
A
  1. too little signaling
    1. myasthenia gravis
      1. cause
        1. autoantibodies against nicotinic ACh receptors
          1. inhibit ACh binding to receptor
        2. cell will enhance the internalization and destruction of the receptor
        3. leads to low levels of functional ACh receptors on skeletal muscle
        4. does not effect the heart
          1. the heart uses muscarinic ACh receptor, which will not be targeted by the antibodies
      2. SS
        1. muscle weakness, muscle fatigue
    2. management-
      1. increase [ACh] signaling
        1. ACh esterase inhibitors
          1. elevates ACh levels
            1. more efficient signaling through fewer receptors
  2. too much signaling
    1. organophosphates - nerve gas, insecticides
      1. cause
        1. irreversible inhibitor for ACh esterase
        2. excess ACh not destroyed
      2. ss
        1. heart muscle
          1. decrease contraction
        2. skeletal muscle
          1. increase contraction
    2. management
      1. -decreasing singaling
        1. block ACh receptors : inhibit ACh signaling
          1. atropine- muscarininc ACh receptor antagonist
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12
Q

list the five major groups of chemical signals and their roles in the body

A

chemical signals

  1. neurotransmitters
    1. source
      1. produced by the nervous system
    2. role
      1. signal transduction through chemical messengers via paracrine communication (very short distance)
  2. hormones
    1. source
      1. endocrine system
      2. types
        1. amine, pepetide and steroid
    2. role
      1. long distance chemical messengers
  3. cytokines
    1. source
      1. produced by the immune system
    2. role
      1. regulate immune function
  4. eicosanoids
    1. source
      1. arachidonic derivatives(prostaglandins, leukotrines, thromboxanes)
    2. role
      1. inflammation, fever promotion, blood pressure regulation, and blood clotting
  5. growth factor- different from hormones how?
    1. source
      1. proteins
    2. role
      1. key proteins that regulate cell growth, signal transduction and proliferation
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13
Q

receptors must be located in anatomical relevance to the chemical nature of the ligands.

Explain the relationship in the body.

What are the types of receptors with in the cell. 3 groups

A
  1. chemical nature of ligand
    1. hyrophobic
      1. pass through the hydophobic membrane
    2. hydrophilic
      1. cannot pass through the hydrophilic membrane
  2. receptor types
    1. intracellular
      1. 1 and 3
        1. 3=estradiol
        2. location
          1. localized in the cytosol in complex with HSPs
            1. this stabalizes the proteins
        3. function
          1. when steroid hormone binds to the receptor, the hsp is shep and the receptors are dimerized
          2. post dimerization the complex translocates from the cytosol to the nucleus
          3. in the nucleus the receptor hormone complex binds DNA with help from coactivators inducing gene transcription
      2. type 2
        1. location
          1. in the nucleus
            1. dimmerized, on element site, with corepressor.
        2. function
          1. hormone passes through the plasma membrane.
          2. passes through the nuclear pore binds to the receptor.
          3. coactivator replaces the corepressor
            1. this structure is now an trancription factor
          4. the quatranary structure is now active and incudeces gene transcription
      3. NO
        1. structure
          1. nitric oxide is a water insoluble product of Arg and O2.
        2. mechanism
          1. freely passes through plasma membrane
          2. activating guanylate cyclase
          3. guanylate cyclase generates cyclic GMP
            1. a second chemical messanger
          4. cGMP increase leads to changes in cell behavior
            1. smooth muscle
              1. causes vaso dilation
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14
Q

Jerry has ulcerative colitis and was prescribed dexathasone as an anti-inflammatory stroid. What is the signaling pathway of the drug, intracellular receptor? explain pathway

A
  1. Dexamethasone
    1. structure
      1. steroid
      2. 30x’s more efficient than cortisol
    2. mechanism
      1. diffuse through membrane
      2. dimmerize with type 1 receptor, releasing bound HSP
      3. receptor-hormone complex translocate to the nucleus
        1. this complex is a quartanary complex that is known as a transcription factor
          1. assists with assembly of transcribing holoenzyme leading to transcritption of a gene
      4. bind to hormone responsive element, DNA binding site
        1. may be assisted by coactivators, secondary super structures
      5. transcibe anti-inflammatory genes
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15
Q

Billy is 150lbs overweight. His doctor tests his HbA1c levels and finds them through the roof. The Dr prescribes him TZD, which activates type 2 intracellular receptors. explain his condition and the mechanism of the drug presribed

A
  1. thiazolidinediones
    1. structure
      1. hydrophobic
    2. mechanism
      1. traverses the plasma membrane, through the nuclear pore.
      2. attaches to fatty acid receptor (PPARgamma) complex and corepressor is swapped for a coactivator
      3. The TF is now active and transcribes potential proteins leading to plasma membrane remodeling and eventually proper glucose transporters
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16
Q

Susan is having a suspected heart attack while the EMR picks her up. She is given nitroglycerin.

How does this drug act and what is the mechanism? what are two other drugs that target the production of this chemical

A

nitroglycerin

  1. function
    1. generation of NO
      1. a water insoluble product
    2. traverses through the plasma membrane
    3. in the cytosol, binds to and activates guanylate cyclase
    4. guanylate cyclase generates cGMP
    5. cGMP is a secondary messanger causing cellualr changes in behavior
    6. causes vaso dilation in smooth muscles

other drugs

  1. nitroprusside
    1. generates NO
      1. lowers blood pressure
  2. hydroxyurea
    1. generates NO
      1. decreasing cell sickling by increase generation of HbF(2alpha2gamma)
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17
Q

what are the three types of surface receptors

  1. receptor
    1. funciton
    2. example
A
  1. ion linked
    1. function
      1. binding of ligand to receptor opens/closes the ion channel
    2. example
      1. nicotinic ACh receptor
  2. g-protien linked
    1. finction
      1. ligand binding induces G protein leading to intracellular cascade
    2. example
      1. adrenergic receptor
      2. glucogon
      3. muscarinic ACh
      4. Rhodopsin
      5. Dopamine
  3. enzyme linked
    1. function
      1. ligand binding activates enzyme
    2. example
      1. insulin receptor
      2. growth factor receptor
      3. interleukin 1- cytokine important for regulation of inflammatory response
      4. integrins - adhesion with the extracellular enviornment
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18
Q

Jerry is on a drug that is an antagonist for nicotinich ACh receptors. What is this drug stimulating? describe the function

A

ion channel linked receptor

  1. function
    1. binding of chemical signal to the receptor/channel opens/closes
    2. convert chemical stimulus into electrical
    3. mediate communications in both the CNS and PNS
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19
Q

Pete is experiencing a cardian arrhythmia and given a beta1 blocker.

What does this drug bind to? describe the general function of this receptor type.

  1. structure
  2. function
  3. example
    1. five
A

G protein linked receptor

  1. structure
    1. 7-transmembrane domain
    2. heterotrimeric G-protein
      1. G= GDP binding)
  2. function
    1. ligand binds to the transmembrane domain, activating the G-protein.
    2. Activation of G protein linked receptor
      1. the quaternary structure seperates and the subunits can activate/inhibit cellular processes
  3. examples
    1. adrenegic -epinephrine, norepinephrine
      1. family
        1. alpha(1,2)
        2. beta(1,23)
      2. function
        1. regulate
          1. heart rate
          2. smooth muscle contriction
          3. metabolism
      3. function
        1. major pharmaceutical targets
          1. beta 1 blockers(antagonists)
            1. ​used for cardiac arrhythmias
    2. glucagon receptor
      1. mediates the metabolic effect of glucagon during fasting
    3. muscarinic ACh
      1. regulates heart rate
    4. Rhodopsin
      1. senses light in the rod and cone cells of the eye
    5. Dopamine-neurotransmitter receptors
      1. function
        1. major drugs to treat
          1. schizophrenia
          2. parkinson’s disease
          3. ADD
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20
Q

What determines the cell response to a sepcific surface receptor?

A
  1. type of receptor
    1. ionchannel
      1. nicotinic ACh- simulate skeletal muscle contraction
    2. g-protein
      1. mediate through secondary messangers
        1. cAMP, cGMP, Ca2+, DAG, IP3
      2. muscarinic ACh receptor - decreases the contraction of the heart muscle
    3. enzyme-enzyme linked
  2. intracellular machinary
    1. even if the receptors are the same, a chemical signal can induce different responses depending on what types of proteins are present inside the cells
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21
Q

G protein and enzyme linked share the surface space of plasma membrane. Whatis different about their stimulation?

A
  1. G protein
    1. induce second messangers through signal amplification
      1. messangers, mostly always, protein kinases
        1. the phosphorylate proteins
          1. enzymes
          2. metabolic proteins
          3. transcription factors
  2. enzyme-enzyme linked
    1. has same targets, but no amplification through secondary messangers
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22
Q
A

most of the time Ga subunit mediates signaling, but the B and Y subunits may particitpate

s=stimulatory

i/o=inhibitory

q=phospholipase via Cbetas

t=transducin

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23
Q

Describe and draw the process from the time of stimulation to the time of resetting.

assume subunit =Gs,a

A

the a subunit can have either a stimulatory (Gs,a) or inhibitory G(i,a)

The g protein has an internal hydrolytic ability to kick off the GDP and reset.

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24
Q

completet the flow chart for a G(s,a) and G(i,a)

A
25
Q

How does cholera effect the cell receptors?

A
  1. cholera toxin transfers an ADP-robose group to G(s,a) subunit
    1. post-translational modification
  2. GTP cannot be hydrolyzed back to GDP
  3. the adnylyl cyclase remains constantly active
    1. leading to lots of cAMP
  4. it causes extreme salt and water efflux from gut epithelial cells to the lumen, causing diarrhea
26
Q

How does pertussis affect the receptors of this system?

A
  1. pertussis toxin transfers an ADP-ribose to a G(i,a)
    1. post tranlational modification
  2. G protein is inhibited from activating and cannot bind to receptor
    1. The normal function of G(i,a) is to turn off adenylyl cyclase.
  3. adenylyl cyclase cannot be inhibited
    1. leading to lots of cAMP
  4. this leads to increased mucus secretion in the airway epithelium and the distinct “whooping cough”
27
Q

describe the processes andenylyl cyclase is repsponsible for. What does PKA do? how is it turned off?

A
  1. structure-tetramer subunits
    1. 2 catalytic
    2. 2 regulatory
  2. function
    1. tetramer= inactive
    2. ATP + adenylyl cyclase =cAMP + tetramer = conformation of regulatory subunits and realease of 2 catalytic subunits
    3. PKA phosphorylate enzymes or gene transcription
    4. reveresed by phosphatases
28
Q

Jim is on two hours of sleep and has red eyes. His clear eyes has an a1-adrenergic agonist in the ingredients. Describe the mechanism starting from ligand->receptor.

list the second messangers3

A

G-protein linked receptors can activate protein phospholipase Cbeta

alpha1-adrenergic receptors on smooth muscle cells mediate vasoconstriction through this mechanism.

  1. messangers
    1. IP3,Ca3+,DAG
29
Q

describe the effect of photons on rhodopsin

A
  1. photons activate rhodopsin(receptor)
  2. rhodopsin activates transducin
  3. phosphodiesterase hydrolyzes cGMP to GMP(degrades 2nd messenger!)
  4. the fall in cGMP levels CLOSES cGMP GATED ION CHANNELS
30
Q

how does the heart muscle react to ACh? describe the process from ligand binding to the receptor.

what makes it distinct from the other G-protein receptors?

A
  1. channel activation is performed by the BY subunits NOT by the alpha subunit
  2. there are not second messengers or kinases involved in this process
31
Q

how is g protein involved in the heart regulation

What role does caffiene play

A

caffeine is an antagonist of the adenosine receptor and increases heart rate

32
Q

describe the three types of enzyme-enzyme linked receptors. Draw and give general principles

A
  1. enzyme-enzyme linked receptors
    1. Tyrosine kinase receptor
    2. JAK-STAT receptor
    3. Serine-Threonine receptors
  2. general principles
    1. dimerize, phosphorylation on receptor, signal transducer protein binds.
  3. function
    1. the receptor has to dimerize to induce intracellular signal transduction
    2. initiating intracellular signaling requires phosphorylatin of the receptor
    3. the phosphorylated receptor binds signal transducer proteins
33
Q

interleukin-1 is sent from an activated T cell, how is this molecule communicated with a recipient cell?

A

The JAK-STAT receptor

  1. strucutre
    1. kinase associated receptors
  2. function
    1. ligand binds, dimerization occurs and JAKs bind
    2. JAKs phosphorylate eachother then the receptor.
    3. receptor binds to and phosphorylates STAT
    4. STATS dissociate from the receptor and head to the nucleus as transcription factors
  3. modality
    1. used by most cytokine for signaling
34
Q

describe serine-threonine kinase receptors

A

serine-threonine kinase receptors

  1. structure
    1. type 1 and 2 receptors interact
    2. SMAD protein
  2. function
    1. receptor subunits interact after TGF-B(example of many) interact with type 2, attracting type1.
    2. after interaction SMAD is phophrylated and used to regulate gene transcription
  3. examples
    1. growth factors
35
Q

describe the funciton and modality of tyrosine kinase receptor

A

tyrosine kinase receptors

  1. structure
  2. Function
    1. growth factor factor bands, causing dimerization
    2. autophosphorylation on tyrosines, intracellularly
    3. adapter proteins attach
    4. complex assembles, RAS (tertiary protein) cleaved of GDP picks up GTP
    5. RAS-GTP binds Raf
    6. Raf activates MAP kinase pathway
    7. this pathway regulates transcription and translation
  3. modalities
    1. used by many growth factors and insulin
  4. can stimulate multiple pathways
    1. MAP-kinase
    2. PLCy (phospholipase Cy
    3. PI-3(phosphatidylinositol-3-kinase
36
Q

After eating a 3 course meal you sit down to study. describe how insulin is used. list the pathways and the funcitons.

  1. clearing glucose
  2. transcription factors
  3. storage/use
A

three possible pathways

  1. PI-3K
    1. purpose
      1. clear glucose from the circulation using GLUT4
        1. found in adipose and muscle
    2. mechanism
      1. PI3K pathway will send all the vesicles of GLUT4 from the circulation very quickly.
  2. RAS-Raf-MAP kinases
    1. purpose
      1. transcribe proteins for glucose metabolism
    2. mechanism
      1. cause the production of metabolic enzymes
  3. PLCy
    1. purpose
      1. regulate the enzymes to generate storage molecules from the glucose.- glycogen and lipids
    2. mechanism
      1. phosphoryate enzymes
37
Q

TZD is used to manage typ2 diabetes, does this activate the pathway from the begning of the cascade? Describe the advantages and disavantages to cell targets

A

signaling pathways do not act alone

  1. disadvantage
    1. interferring with a pathwasy can cause side effects in other pathways
  2. advantage
    1. an alternate pathway can partially restore the function of an impaired pathway
38
Q

undersignaling and over signaling can be a huge problem for cellular communication. How is this regulated by the cell?

there are 5 mentionables.

  1. ACh esterase
  2. hormones change the regulation of other hormones
  3. desensitization through phosphorylation
  4. phosphodiesterase
  5. phosphatases
A
  1. destruction of the chemical signal
    1. ACh esterase destroy ACh
  2. decreased synthesis of the chemical signal
    1. negative feedback regulation of hormone synthesis in the hypothalamus and the pituitary gland
  3. reduction of the functional receptors
    1. desnsitization of some receptors by phosphorylation
      1. binding of the signal to the receptor no longer results in signaling
    2. removal of receptors from the cell surface by endocytosis
  4. destruction of second messengers
    1. phsophodiesterase destroys cAMP, cGMP
  5. reversing the effects of kinases
    1. phsophatases remove phosphate groups from proteins
39
Q

Janice was diagnosed with graves disease. What is the normal regualtion of the pathway between hypothalamus, anterior pituitary and thyroid gland? How does graves disease interupt this pathway.

A

hyperthyroidism (Graves disease)

  1. autoantibodies stimulate TSH receptors in the thyroid gland, leading to increased hormone production
  2. Thyroid hormone downregulates TSH production but has no effect on autoantibodies
  3. the negative feedback does not work
    1. the thyroid gland is stimulated by the autoantibodies, generating thyroid hormone even though there is no TSH.
40
Q

Jim has a tumor in his pancrease that is increasing the amount of glucagon in his system. What receptor will be overstimulated?

A
  1. Glucagon G protein receptor
    1. mediates the metabolic effect of glucagon during fasting
41
Q

diffrentiate the 3 basic pathways of trimeric G-protein signaling

give the response enzyme, list ligand and steps to activating this enzymes.

A
  1. adenylate cyclase
    1. activation by G(s,a)
      1. increases cAMP
    2. inhibition by G(i,a)
      1. decreases cAMP
  2. protein kinase C
    1. upstream ligands
      1. a1-adranergic agonists
    2. activation-Cbeta leads to release of secondary messengers
      1. steps
        1. Gprotein(a1-adranergic receptor) activate
        2. phospholipase C-beta cleaves IP3 from DAG
        3. IP3 stimulates release of Ca2+
        4. DAG and Ca2+ binds to PKC and activates it
  3. ion channel
    1. phototransduction
      1. upstream ligand
        1. light stimulates rhodopsin
      2. steps
        1. photon activates rhodopsin
        2. rhodopsin activates transducin
        3. alpha unit activattes a phosphodiesterase
        4. P-esterase hydrolyzes second messenger
          1. cGMP->GMP
        5. cGMP/GMP ratio <<<1 = closes cGMP-gated ion channel
    2. muscarinc
      1. ligand
        1. ACh
      2. steps
        1. ACh binds to muscarinic ACh receptor
        2. Gby dissociate from G(i,a)
        3. Gby opens a K+ channel
        4. NO SECCONDARY MESSENGERS
          1. exception to the usual 2ary messenger seen in most
42
Q

list characteristic examples of drug groups that affect the following signaling pathways

  1. neuromuscular junction signaling
    1. drug-condition
      1. info
  2. nuclear receptor signaling
  3. nitric oxide signaling
  4. adrenergic receptor
A
  1. neuromuscular junction signaling
    1. ACh inhibitors-Myasthenia gravis
      1. elevate ACh
    2. Atropine-organophosphates
      1. block ACh receptors
        1. inhibit ACh signaling in area
        2. important for muscarinic ACh receptor
  2. nuclear receptor signaling
    1. Dexamethasone-inflammation
      1. steroid drug acts through type1/3 intracellular receptor.
      2. 30x’s more efficient than natural cortisol to decrease inflammation.
    2. TZD-type 2 diabetes
      1. Activates PPARy pathway, increasing insulin sensitibity
  3. nitric oxide signaling
    1. Nitoglycerin/nitroprusside/hydroxyurea-heart attach
      1. decompose to nitric oxide and cause vasodilation
  4. adrenergic receptor
    1. B1 blockers-cardiac arrhthmias
      1. block the B1-adrenergic receptor
        1. normal, with out the blocker
          1. G(s,a) -> adenylate cyclase (on)-> increase cAMP= increase heart rate
    2. a1 adrenergic agonist-red eye
      1. eye drops used as a decongestant. to vasoconstrict.
      2. pathways
        1. PKC pathway
          1. G(q,a)->phopholipaseCB-> IPS,CA2+,DAG->PKC
43
Q

receptor for cortisol

A

Type 1 intracellular

44
Q

receptor for adosteron

A

type 1

45
Q

receptor for progesterone

A

type 1

46
Q

receptor for testosterone

A

type1 intracellular

47
Q

receptor for estradiol

A

type 3

48
Q

receptor for dexamethasone

A

type 1/3

49
Q

receptor for throid

A

type 2 intracellular

50
Q

receptor for vit D3

A

type 2 intracelluar

51
Q

receptor for retinoic acid

A

type 2 intracellular

52
Q

receptor for fatty acid

A

type 2 intracellular

53
Q

receptor for TZD

A

type 2 intracellular

54
Q

receptor for NO

A

intracellular guanylate cyclase-cGMP

55
Q

receptor for dopamine

A

G protein receptor

56
Q

receptor for rhodopsin

A

G protein open cGMP gated channel, via cGMP

57
Q

receptor for glucagon

A

G(S,a) adenylate cyclase

58
Q

receptor for adrenergic

A

G protein linked receptor

59
Q
A