Flashcards in Cell Signaling Deck (59):
What are some examples of Neurotransmitters?
What is the release of neurotransmitters released by?
What type of channel does acetylcholine acitvate?
has dual function
neurotransmitter and a hormone
Where is hTERT seen?
most human tumors
endless growth in cluture
Cell Signaling Molecule Types
cell responding to signals that they produce themselves
secrete prostagladins and interleukins
ex. GF (if unregulated leads to tumors)
signals that are acting locally
can bind to oen or more receptors
secrete hormones and growth factors
ex. neurotransmitters at synapse
Examples of Paracrine signaling genes
fribroblast growth factor
transforming growth factor and super family
secrete polypeptide and steroids into blood
distant target cells
Steroid hormones circulate in blood bound to what?
Steroid hormones can be adminstered
steroid hormones are administered from
Steroid hormones are (stored/or not stored) in producing endocrine cell?
Steroid hormones bind to what type of receptors
Are steroid hormones polar or non polar
(hydrophobic) diffuses across plasma membrane
are all examples of...
ex steroid hormones
corticosteroid is produced by
cortex of adrenal gland
There are two types of corticosteroids
glucucorticoids( stimulate production of glucose)
mineral corticoids (act on kidney to regulate water and alt balence)
What type of signaling molecules bind to intracellular receptors?
Retinoids ( syn by vitamin A(
Does NO cross the plasma membrane?
Yes. but it does not bind to intracellular receptors instead it REGULATES ACTIVITY OF INTRACELLULAR TARGET ENZYMES.
what type of cell signaling is NO?
what is NO made from
arginine and nitric oxide synthase
dilation of the blood vessels
Steroid Hormone Process
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
Name the Cell surface receptors
blood platelet aggregation
smooth muscle contraction
Examples of Eicosanoids
What are eicosanoids synthesized from?
Asprine and anti-inflammatory drugs have an effect on ....
they inhibit prostagladin synthase
Examples Peptide hormones
peptide hormones (insulin, glucagon, hypophysis hormones)
Neuropeptides (enkephalins and endorphins)
What do Enkephalins and Endorphins do?
decrease pain in the CNS
how do peptide hormones circulate in blood?
circulate in blood as unbound vesicles
How are peptide hormones stored?
membrane bound secretory vesicles
precursor molecules (prohormones)
Peptide hormones are polar or non polar?
polar (water soluble)
Peptide hormones bind to ...
cell surface receptors
Can peptide hormones be administered orally?
What are examples of Intracellular signaling pathways ?
pospholipase C-Ca pathway
Describe cAMP pathway
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
Describe phospholipase-protein kinase C-Ca pathway
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
Describe tyrosine kinase receptors
They are activated by GFs and insulin
they are transmembrane proteins
they are surface receptors
What does imatinib mesylate affect?
tyrosine kinase receptors
it binds to atp domin and prevents downstream signaling
Steps of tyrosine kinase receptor?
1. binding of ligand (GF) to extracellular domain
2. receptor dimerization
3. receptor autophosphorylation
Two types of domain of tyrosine kinase receptor?\
extracellular domain ( ligand binding)
intracellular kinase domain (catalytic)
What are cytockine receptors?
not instrinsic componenets
intracellular tyrosine kinase
NF-KB TF pathway
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)
cytoplasm and nucleus
recognizes proteins with attached ubiquitin (degraded in chamber)
proteins degraded in barrell
ERK- MAP KINASE PATHWAY
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
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
contained in niches of stromal cells
lose intracellular ahdesion
break down into apoptotic bodies ( are phagocytosed by macrophages and inflammation doesnt occure)
non-phsyiologic after acute injury
lyse and release cytoplasmic and nuclear contents into the environment
inflammatory response occurs
Signals of 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
a capsase also cleaves BID (BCL-2 family)
b. BID enters the mitocondria and triggers the release of cytochrome C
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