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INTRACELLULAR RECEPTOR AND CELL SURFACE(TRANSMEMBRANE)

okie so basically

there is ab abodnant amounto f pshohoglycerides whcih are a group of falmily form phoshlipdis - these phoshplipds had heads tails, tials stuared, unstatured kinks, striaght and stured long meansin less lfuidity visfcotity to the membrane , the unstated short means better fluidityn , higher and higter movments means more fluidity. these phsohlipds glucerdes there subsets. glycerides called phsohoadtylserine and pshsoatylcholine. serine is in the cytoplasmia dn cfhokini s nt he explos. cholestorl is in the mbernae evently distbutede, atty aicfe and amipaothi ike the rest bc of th oh gorup tht is istikign out. thes pshoatdyls rines are for helpign hte insl stranmit it kind of like stablizes the memrbame. the disbturtiono f the ps is important becasie it dtermiens if the cell dies or ot. so absically flipasewill use atp to flip the serine to the exoplasmic side of the memrbane and thsi epose it to macrphages that will bind and macophages are suaully running around the bloodstream. and phaocyte them and apoptsis them. so the disorganization pf te membrane will lead to apoptosis. the lipds mvoe laterally and rotate around. but it doesnt always indicate apoptisis becaus iet cna be b ecause the cut and tit spaotydedsrine ocmes out to makg clotting. the way to sytudy thsi is through frap where we take a live cell put oloring emnrbane ucne the signl iwth a ray ad te osberve how much is removed. we will observe mobility and inbolity. we got thre dif tyeps of proteins. transmebrane, peripheral, adn lipid anchor. transmber three domains. . oh i forgot that lipds are help by weak van der waal interactions and weak hydrophobic. interactiosn. and we got lipd anchor. there covalent linkages that hold the fuck as lipd anchor so basically we eitehr preylate them or acetylate them prenyl is held by lipid though a c temrinl and the actyl is though the n terminal so the prenyl si called farnesyl . the target protein has cystein, two alipathic (hydrophobic) ala val and leu and we got a random X. and we get a prpenul and it is added by a prenyl transferase through the cystein and the carbon and it through a covalent bond making a thioether and then it will attach. so then caax protease will remove the last three and create a negative charge . then methyltranserase will neutralize it because we need it to neturalize to be a smother connection ot the membrane. so then it binds because its hydrophobic and nets to be attached. transmembrane proteisn are homdimers. this is post tranlational. modifiation. 

single pass tranmembta glycophroin is a single pass . and homodimer. so 

so singal recpeotrs can be surface recpeotr (tranmamberane ) and intracelular recpetors that 

OKIE

soooo transmembrean proteins can be cell surface, and intracellylar can be peripherial or anchor inside the cytosol. 

intracellular receptors are inside the cell and can pass hydrophobic molcules and cell surface are for the hydrophilic. OKIE so intracellular for hydrophobic and so t a way that a 

a way that a cell responds o these singling evnets i through singal tranduciton process. the recepto will recgvonize those singling mocluels called ligan. a singling recpetors menin either 

surface receptors are transmembrean and intracellular are inside the cytoplasm moclules. so there are singling recepors either in the inside which are intracellular and take in ligand that are hydrophobic. cell surface receptors tak in

cell surfac ena dperipheral are different cell surface take in hyodrphili and intracellular are the phobic ones. so when a ligan binds confirmatoin change happens and increases the affintiyt for downstream singling moclule to bind. 

without the ocnrimation change the affinity is much lower. the lock key meachsni is that the mocleul completnary of ligand and recepto then ther eis the mocleualr swithc it is  the conrimtaion change that happens when a ligan d binds. 

there are four types of singals - endocrine -paracrine - autocrine and ligand bound receptor. the more receptors present to the rligand the better teh signal . 

there are super family - 

nuclear receptor super family are intracellular - transmembran homone recedptors

cell suface receptors which are enzyme voupled ion channe and g protien\\

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wthere are families the nucelare receptor are the itnra cellular 

cell surfcace are g coupled trans emrbean

enzyme coupeld receptors are homdimers like rtk which is a kinase that prhoylates it s a trans autphrooylated 

okie so rtk binds to a growth factor then it will dimeraze then it will rphoyalte itself then the grb2 will bind because its sh2 will recognize the source whcih is the rtk receptor and then bind to the sos which is twhat is held b the sh3 domain. sos is sons of senvelness then it binds and this is where it will bind cry and die. then biding sos to the fuck ass ras gdp whichi s of and itll act like gef and remove the gdp. to fall off and then it will make it into the gtp thi sis hwer eit becomes gtp and then after ebcomign gtp it will have higher affinity for nactive raf and raf has 14-3-3- and falls off and then that binds to the mek then mapk so they all phrohoylate eachother. lalala la and then it goes inot the neucleus and then it psohoylates the TF and get shte gvnes ogoing. cancer can hhijak the system and causes proliferation for the long run thisn si really bad. there are hundred of tyrokinase in the body receptors and not all can work for all recpetors. kinase reoznises the maino acids they prhoylate like 6-8 even if two proteisn have tyosin the surround smino acids demrien it he kinase cna proylat eit. 

grb2 i s a mediated since it has the sh2 and 3

ras is a protoconco but can become oncogene when hgih lactiivated causes caner and tumor supress is phrotase which can dephoyalte and igap can also act as it and stop hyperactivity and 14-3-3 but photase acts as a turmo supressor. 

there are iosmers of the ras whcih are hras or kras 

the studicnets study the ras/map tranduction pathway through the drosphilia fly bu looking at the fuck ass ocmpodun ommtidium which has 22 cells but 8 neruorh photosenorsy cells and the r8 is made fisrst then it will diferenatiate the rest. so there si s ar7 mtatuoin that will lead to the lack of being able to see uv . and so basiclly the r8 is made first and the ligands ofr ht erest of the surrounding cells are …. …… … ….. ………………………………….. taking in the ligand which is on the receptor of the r8 this ligand is claled BOSS bride of sevenless bowss binds to the r7 sevenless receptor and hten it will phrohoylate itself and then have something that is like a grb2 moclule (called drk) and also has a sh2 domain called 2sh3 which will bind and bind to the ras -gef which will turn on the ras trandcution. ras gef isis like. a SOS