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HIstology > Cell Signaling > Flashcards

Cell Signaling Flashcards

1
Q

What are some examples of Neurotransmitters?

A 
acetylcholine
dopamine
epinephrine (adrenaline)
serotonin
histamine
glutamate
GABA
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2
Q

What is the release of neurotransmitters released by?

A

Action Potentials

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3
Q

What type of channel does acetylcholine acitvate?

A

ligand gated

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4
Q

Epinephrine

A

has dual function

neurotransmitter and a hormone

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5
Q

Where is hTERT seen?

A

most human tumors

endless growth in cluture

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6
Q

Cell Signaling Molecule Types

A 
Autocrine
Endocrine
Paracrine
Neurotransmitter 
neuroendocrine
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7
Q

Autocrine signaling

A

cell responding to signals that they produce themselves
secrete prostagladins and interleukins
ex. GF (if unregulated leads to tumors)

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8
Q

Paracrine signaling

A 
signals that are acting locally
can bind to oen or more receptors
secrete hormones and growth factors
ex. neurotransmitters at synapse 
glucagon
somatostatin
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9
Q

Examples of Paracrine signaling genes

A

fribroblast growth factor
hedgehog
wingless
transforming growth factor and super family

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10
Q

endocrine signaling

A

secrete polypeptide and steroids into blood
distant target cells
ex. neuroendocrine

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11
Q

Steroid hormones circulate in blood bound to what?

A

proteins

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12
Q

Steroid hormones can be adminstered

A

orally

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13
Q

steroid hormones are administered from

A

cholesterol

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14
Q

Steroid hormones are (stored/or not stored) in producing endocrine cell?

A

not stored

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15
Q

Steroid hormones bind to what type of receptors

A

intracellular

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16
Q

Are steroid hormones polar or non polar

A

non polar

(hydrophobic) diffuses across plasma membrane

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17
Q

Testosterone
estrogen
progesterone
are all examples of…

A

ex steroid hormones

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18
Q

corticosteroid is produced by

A

cortex of adrenal gland

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19
Q

There are two types of corticosteroids

A

glucucorticoids( stimulate production of glucose)

mineral corticoids (act on kidney to regulate water and alt balence)

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20
Q

What type of signaling molecules bind to intracellular receptors?

A

Steroids
VitaminD
Retinoids ( syn by vitamin A(
Thrroid hormone

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21
Q

Nitric oxide

A

signaling molecule

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22
Q

Does NO cross the plasma membrane?

A

Yes. but it does not bind to intracellular receptors instead it REGULATES ACTIVITY OF INTRACELLULAR TARGET ENZYMES.

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23
Q

what type of cell signaling is NO?

A

paracrine

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24
Q

what is NO made from

A

arginine and nitric oxide synthase

25
Q

NO causes

A

dilation of the blood vessels

26
Q

Steroid Hormone Process

A
  1. hydrophobic steroid hormone cross plasma membrane
  2. steroid hormone binds to cytosol receptor
  3. steroid cytosol receptor goes inside nucleus binds to DNA changes gene expression
  4. activation or inactivates
27
Q

Name the Cell surface receptors

A

Peptides
Neurotransmitters
Eicosanoids/Leukotrieinds

28
Q

Eicosanoids Function

A

blood platelet aggregation
inflammation
smooth muscle contraction

29
Q

Examples of Eicosanoids

A

prostagladins
prostcyclin
thromboxanes
lekotreines

30
Q

What are eicosanoids synthesized from?

A

arachidonic acid

31
Q

Asprine and anti-inflammatory drugs have an effect on ….

A

eicosanoids…

they inhibit prostagladin synthase

32
Q

Examples Peptide hormones

A

peptide hormones (insulin, glucagon, hypophysis hormones)

Neuropeptides (enkephalins and endorphins)

GF
cytokines

33
Q

What do Enkephalins and Endorphins do?

A

decrease pain in the CNS

34
Q

how do peptide hormones circulate in blood?

A

circulate in blood as unbound vesicles

35
Q

How are peptide hormones stored?

A

membrane bound secretory vesicles

36
Q

Peptide hormones..

A

precursor molecules (prohormones)

37
Q

Peptide hormones are polar or non polar?

A

polar (water soluble)

38
Q

Peptide hormones bind to …

A

cell surface receptors

39
Q

Can peptide hormones be administered orally?

A

No

40
Q

What are examples of Intracellular signaling pathways ?

A 
cAMP
cGMP
pospholipase C-Ca pathway
NF-KB pathway
Ca-calmodulin pathway
MAP
JAK-STAT
41
Q

Describe cAMP pathway

A
  1. cell receptor binds hormone
  2. g protein activated (GDP to GTP)
  3. alpha subunit leaves and phosphorylates adenyl cyclase
  4. adenyl cyclase transforms ATP to cAMP
  5. cAMP binds to regulatory subunits of PKA
  6. PKA catalytic subunits go into the nuclus and phosphorylate CREB which is attached to CRE
  7. gene expression continues
    * cAMP is degraded by cAMP dep. phosphiesterase
42
Q

Describe phospholipase-protein kinase C-Ca pathway

A
  1. Activated PROTEIN KINASE DOMAIN (DIMERIZED)
  2. phospholipase C gamma is phosphorylated with its SH2 domain
  3. which catalyzes the hydrolysis of PIP2 to DAG and IP3
  4. DAG activates PKC
  5. IP3 activates the release of calcium
43
Q

Describe tyrosine kinase receptors

A

They are activated by GFs and insulin
they are transmembrane proteins
they are surface receptors

44
Q

What does imatinib mesylate affect?

A

tyrosine kinase receptors

it binds to atp domin and prevents downstream signaling

45
Q

Steps of tyrosine kinase receptor?

A
  1. binding of ligand (GF) to extracellular domain
  2. receptor dimerization
  3. receptor autophosphorylation
    4 SH2
46
Q

Two types of domain of tyrosine kinase receptor?\

A 
extracellular domain ( ligand binding)
intracellular kinase domain (catalytic)
47
Q

What are cytockine receptors?

A 
Src Family
JAK
GF
not instrinsic componenets
intracellular tyrosine kinase
48
Q

NF-KB TF pathway

A

heterodimer

  1. (NF-KB) forms a dimer with (I-KB) which is inactive
  2. PKC activates said dimer and breaks it apart
  3. (NF-KB) is translocated into the nucleus where it regulates gene expression and the phosphorylated (I-KB) is sent to the 26s proteosome (phosphorylation dependent degradation)
49
Q

26S proteasome

A

protease
cytoplasm and nucleus
recognizes proteins with attached ubiquitin (degraded in chamber)
proteins degraded in barrell

50
Q

ERK- MAP KINASE PATHWAY

A
  1. growth factor binds to (growth factor recognizing domain)
  2. RAS-GDP which is attached to RAF becomes phosphorylated and becomes RAS-GTP
  3. The RASE-GTP/RAF complex phosphorylates the MEK complex
  4. the MEK complex phosphorylates the ERK complex
  5. the ERK complex translocates in the nucleus where it phosphorylates the ELK-1 (TF)
  6. The new phosphorylated ELK-1 TF now can bind to SRE AND SRF which leads to gene induction
51
Q

JAK-STAT PATHWAY

A
  1. cytokine receptor is activated
  2. JAK PROTEIN tryosine kinase is activated therefore STAT binds to it
  3. after the binding of STAT to JAK protein it becomes phosphorylated
  4. the phosphorylated STAT Protein forms a dimmer with another phosphorylated STAT protein which translocates into the nucleus
  5. gene transcription activated
52
Q

Stem Cells

A

proliferation
self renewal
differentiation
contained in niches of stromal cells

53
Q

Apoptosis

A

lose intracellular ahdesion
fragment chromatin
break down into apoptotic bodies ( are phagocytosed by macrophages and inflammation doesnt occure)

54
Q

Apotosis proteins

A

Apaf
BCL-2
BCL-2 (3)

55
Q

Necrosis

A

non-phsyiologic after acute injury
lyse and release cytoplasmic and nuclear contents into the environment
inflammatory response occurs

56
Q

Signals of Apoptosis

A 
external
TNF-alpha
Fas Ligand
internal
cytochrome c
57
Q

Fas Ligand

A

intiates apoptosis
binds to FAS receptor(aka APO1/CD95)
3. causes trimerization which with the help of FAD recruits
4. procaspase 8 and turns it into caspase 8
5. caspase 8+Fas receptor +FADD forms DISC
6.caspase 8 turns procaspase 3 into caspase 3
7. caspase 3 turns ICAD into CAD
8. CAD goes into the cell nucleus and breaks down chromosomal DNA

other part
a capsase also cleaves BID (BCL-2 family)
b. BID enters the mitocondria and triggers the release of cytochrome C

58
Q

Mitocondria

A

signals apoptosis by the release of cytochrome c

1BCL-2 blocks BAX
2 which in turns release cytochrome C and SIMPS into the outer mitocondrial matrix
4. SIMPS AND cytochrome c interacts with Apaf-1
5.this forms aptotosome : apaf-1+atp+procaspase 9
6. procaspase 9 is activated by apaf-1 turns into caspase 9
capsase 9 activates capsase 7 and capsase 10 which leads to prolytic destruction

59
Q

AIF

A

used for apoptosis in the absence of caspases

HIstology (17 decks)

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