Cell signalling proteins

wudiwida's version from 2018-06-24 09:49


Question Answer
Tsc2 (GAP)Inhibits Rheb
Rheb Small G protein activates mTORC1
Cell migrationRac dominates polymerization (forward), Rho dominates cytoskeleton contraction (back)
Grb2bind to SH2 domain on tyrosine kinase and recruits Sos (Ras-GEF)
IRS-1Recruits Grb2
Akt (PKB)activates glycogen synthase, GLUT2 translocation, lipogenesis,
PDE3Brepresses cAMP
Sec23/24Exocytosis from ER
COPIIcoats the vesicle released from the ER to the golgi
PDZ1, YAP65 and c-YESCFTR pathway to ENaC inhibition
cGMPion channel conductance, cell growth and apoptosis and mobility and contractability
PKGsmooth muscle relaxation, platelet inhibition, changes in gene expression
ANP renal excretion of NaCl and H2O, vasodilation and vasculature permeability. Released in high blood pressure
NOS3Nitric Oxide Synthse
PDE5represses cGMP
AmilorideInactivates ENaC
AldosteroneActivates ENaC biosynthesis, tracking and cleavage, channel gating and endocytosis
FurinOne of the proteases for ENaC activation
ProstasinOne of the proteases for ENaC activation
Nedd4-2Ubiquitinase for ENaC
Liddle's Syndrome Loss of ubiquitinating site for ENaC
3 Main K channelsInward rectifiers, Leak channels, Voltage gated
Kir 6.1 / KCNJ8cardiac inward rectifier K channel alpha subunit pore
SUR1beta subunits for inward rectifier K channel ligand binding site
ROMKmajor K secretory channel in the nephron
Bartter’s Syndrome defect in the thick ascending limb of the loop of Henle, characterized by low potassium levels (hypokalemia)
RyR1IP3 receptor but coupled to Cav1
DHPDrug that blocks Cav1.2
Brugada SyndromeLoss of function of SCN5A causing LQTS
SCN5ASodium Influx channel in the heart
KSR1Brings Mek to Raf but moves away after erk binding
SLC4A1 (Band 3)Regulates HCO3- release and important cellular anchor
SAOheterozygous disease where Band 3 cytoskeleton binds more tightly
SLC26A3Transports salt uptake with Na and H
SLC26A4HCO3- secretor and iodine transporter

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