Midterm Cell Bio

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embrane structure

mmmm cellulose
Permeability
oflipidbilayer electrochem gradient

buildingblocksoflife Glucose
four Hydrophobic 0202 continueuntilequilibrium

Adenosine nucleotide
and canformcomplex Alanine
smalluncharged jours GMCc CaCa

Myoglobin

Oleicacid lipid bilayer largeuncharged stages dependoncharge move
to
most lipidare fattya cid
Vm O Vm0

ion 2 titrant

going Infaffiffe't's oof r omfgaF me aiigoieiiiiiisoioanmiitiiiieeriodn.ie


swell shrink

glycerol phosphate10 0

In tail fattyacid zwitteronion transportation Ionophores smallmolecule

Transporter slow strong


transporter andchannel
interactionexposeonlyoneside

PClipidwithfattyacidsof differentlengthwhichdetermine uniporter Symporter Antiporter



thicknessof thebiological membrane significant function
the to

phingolipids

notexistin prokaryote
does pump alternativegates

ceramide aminebond needenergy coupled ATPpumplight
e

g
sphingomyelin cerebrosideganglioside
egglucosetransporter uniportor

polar h ead d when glucosebindstocentralcavityth
OO
t an transporttotheso
sterol
rigid rings conformationchange glucosetrapped

festerol haveOHgroupinoneposition otherside

0PMtail At lowerconcentration transportermediatedworkbetter
ipidassembly
proteinisdifferentsoasfunction
phospholipidbilayer

micelle
this showsthatglucose m ore but
poorly 9Ph
the
hydrophobictails with
contact waterenvironment
so itis graph former
sufficient

unstablesoitmerelytostaylike Miccellewherehydrophilic Glucosecanactassymportersuch as chloreraincidentwherea



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11 in fromthegutlumenandthenouttotheextracellularfluidon
mostfundamental0 618

theothersidethat'swhywedrinkelectrolytetomoveioninthe cell

Bicarbonatechloride antiporter HCG in
4 outviaAEIprotein
lipid

shape CFTR

cone Eaff
pumpCat change ATP
conformation hydrolysed transport

Calcium


cylinder Ufpump ABC MDR
Oag

Channel protein fastporealwaysopendowngradientions



cone id IonChannelsinglegate
selectivefilter

Temperature change incharges
voltagegated

solid ligandgated intra extracellular
substanceattachthen openkio
liquid crystal liquid

Mechanicallygated need forces
partiallyorganised

Aquaporin
e

g havealignstructurewithHaosocantransport


Avoltagechange detect
channel
and open transportht

Nicotinic chattel

acetylcholinereceptor
leaking Kt
musclecontractioninbrain
alwaysopenfork 1tomove

mutationchannel
causesdisease outside

Cl sonegativitycanbe
cysticfibrosis balance
andcontrol

HERG arrhythmia

Navy5 arrhythmia
Caveolae

dimer 6 fatty18

by makes
formed Caveolin

tobend
cholest
raftsunusualarea
which cavedaprotect

cellfrommechanicalstress swelling
eg

socelldoesnotbust

cellularcompartment
ra

unrununurn
Endoplasmicreticulum out

compartmentcan be
differentsize neverisolated AlbertClaude posttranslationalmodification ofproteinin El
receptorcomplexorganellelipiddroplet George Palade Glycosylation sugar is attachedtoaminoacid

enzyme attachglucoseintomoleculeglucoseisadd
de
Christian Duve
quawillidentifyand

proteasome degradeintoothersmaller
compartment
1974
andtrimone onewhilefolding
Calnexinrecognisecarbohy
oithelialcelldistinctsurfaceandasymmetricalplasma
membrane by protein glucosetrim

so itcanfoldproperlyCanchorb oth the1a

Apical Basolateral functiondifferentlysoasymmetrical glucosethenexport
Ebronlongdistancethey havetheirown functionAxondendritenucleus

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opologically identicalsoitcanmove vesiclefusesthe
membrane H reduced
sit

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ppIT ppIf iDIE
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mechanism

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Gated transport large
canformorrearrangeby oxidation reduction
ofppg
oxidise

proteintranslocation transportacrossmembranebetweencompartment
0
qualitycontrol ifnotfold properly refold ordegrade
packagein vesicle allowstotransportmany proteins
0
Vesicular transport proteolysis

Ucleus

lipidsynthesisandtransfertosmoothER morethanother side
2
membrane nuclearenvelope connected toER createphospholipid asymmetrye making
g Rothman
James
cytosol nucleusare topologically
identicalsostuff canmoveinfout

nucleoporins
Vesiculartraffic RandySchekman
nuclearporehavenuclearcomplex
steps 1 Buddingand
fission Thomassiidhof

NLS nuclear l ocalization e


signal g T antigen showsfluresence 3 2 vesicletransport zon3

3 vesiclefusion
GTPase

molecularswitch
activateGDPtoGTP conicallipidPEMPs PC BARproteins

GEFis usedto amembranebending adding
slowsoGAPisneedtoconvertGTPtoGDP

Thisreaction isvery 3majorcoats
Nuclearimport clathrin Plasmamembrane

come in andthe gelstructuredissolveto

proteinwith
NLS Copt Golgi
throughA smallGTPproteincallRan GTP

liquidsocargo can pass
cop s ER
Mandoinstriction

state kickouttheprotein putitselfinand



initsactive
clathrin
nucleuswithcargo High speed moleculeattachtocargo receptor adapterproteincome inandbring

gooutof clathrin triskelion membrane c
by
onstrict dynamin coat remove
GTPase providesdirectionalityfornuclearimport
export

Ran lipid induced conformation switching Ap2
nucleus changeGDPtoGtp hydrolysedtoADPsoenergy

Rah GEF activated only in Auxillin attach Hsc 7 0 ATP altach and
doplasmicreticulum isuseto the
break triskelion and vesicle disassemble

RER SER

Iniron add
use sucrose centrifugation cope
signal Hypothesis at N terminus as signal factor thatstartthisisGTPSarl cargogetattachtoreceptor

membranestart bend cop coatedvesicleforms
to

signal peptide
Cfd TodissociateGtphydrolyseditselftouseenergytobreak
vesicle


Signalpatch formsareathatis Membranefusion

2typesof proteintranslocation agg recognisespecific
protein
4components 4steps
teenager a priming SNAREdisasemble
aSNARE a vesicleby Rab
Co
translational
sonprotein 2Tetheringassociationof
protein

3 RabproteinGTP 3 Dockingmeetanother SNARE and form comp
stable
Howtopushproteinin a fusion

ATPfromribosome
4 SNARE c omplex


ATP ADA
BiP which Pi Golgiapparatuscisface ER transface othercompartment

cisternalmaturationmodel ER Golgi transface

vesicletransportmodel ER cis fuseatmiddle trans

Regulatedsecretorypathway

Endosome early mature late vesiclecanform mechanism


proteintranslocation

vesicle insideendosomeand virusparticlesaremade by similar

J
Tay.gg

gntanehfebreahf
e insertionofGM exosomesbody fluid releasedbyall

2 otherparts comes in b
peptide ond cleaved lysosome degradation ofprotein lipidhighacidhydrolase
reaches hydrophobicareait
disaciate

when it peptidasethenlaterdegraded byGM and form MbpinGolgi bindtoMbereceptor endosome dissociateatanpH

by
signal phagocytosis endocytosis macropinocytosis autophagyeating other
Type 2 peroxisome oxidationorganellesfoundAcone inliver

NHIisoutside
translocation peroxisome fission daugtherperoxiso
His

internal anchor sequence ER

TypeN SNAREISMcycle

have lots of transmembrane
SNAPEassemble fusionporeexpansion

IN fusionporeopening membranefuseSNAREdisasembl

tochondria feedbackmechanism

2membraneouter fatlargeporevery
are
permeable
positivefeedback amplifythiscascade
inner large ASA NICOSregulatebending
interspace crista sofmelimestosillate

oxidativephosphorylation NHzdetox feedback inhibit mechanism


negative

Camheathomeostasis Apoptosis
ROS samesignalbutdifferenttargetsodifferentresponse

their genome 16h
have

own large plasmic bp ribosome


e.g acetylcholine pacemaker salivaskeletalmusle
dividebutnotfromscratch

extremelydynamiccan cellcommunication plasticity
Receptorsequestrationreceptorisremovebyendosomeinside

independentorganellebutcontactconstrictionwithERforfission

fromone
move celltoanotherbynanotubebesorequiremoreATP R downregulation degradedanddigestbtransducer ylysosome
Receptorinactivationresponseisinhibit by orby

oteinimporttomitochondria inhibitoryproteinornegativefeedback

signalsequencerecognisedbyTOMcomplexandTIM 23complexand exampleofimportantmechanism


heymove in to 2
membrane same
at time Cleavagebysignalpeptidase NOeasilycrosspmandactivateSGCtochangeGTPtocGMP

Nath passingthroughligandgated
channeland canchange
ell communication

muumuu theconformationoftropomyosinallowing musclecontraction


attractant sensestimuli
chemo andmovetowardtheenvironmentofAcone

repellent sensestimuliandmoveaway
chemo Basicmechanismofsignaltransduction cell
of

specificityamplification modularity desensitizeintergatelocal
acteria

producesignallingmoleculewhichcan tellhowmanytheyare cancer cellcannotfunctionmultiplechangesoccurs

eukaryote singlecellaggregatetogetheras timegoesooo8 Gogo Herceptin antibodywhichinhibitsignal forcellgrowth cant


g
Sbacteria
rosettacells CART celltherapy geneticallychange reprogram cover

secrete
enEiimewhich signal
is to make them aggregatetogether
synapses
and thesingle cell fuse nuclear f usion meiosis winesiteforneuronal
communication synaptic cleft

juxta action potential

ender signal reliever brainnetwork memoryandcognition muscle


affectbehaviourfunction excitation movein causede polarisation contra

for
hats other hormoneneurotransmitter
inhibitation 0 movein or vesa v ise membrane hyperpolarised

decoding when itrelievethesignalitstartedtodecodeandextractthe secondmessenger have complexaffect onexcitlinh

y
meaning something willhappentothecell migration modulation
Electricalsynapse foundinbraingap junctiononlyexcitation

9 pA
cadiIeerrYinfuesignnmaiMmestinmsdiaia.e
rentfunction zfinemical synapse
Action
neurotransmitter

potentialreachessynapticterminal
bindstosynaptotag

divide diffentiate
openofthevoltagegatedchannelofCa24
second
Typesofcommunication
messenger

rapidentryofCaatopresynapticterminal
0Contact gapjunctionfor
dependent electricalactionpotential

Juxtacrine inducevesicletoreleaseneurotransmitter releasetosynapse

rightnexttoeachotheregheartmuscle
receptorofpost synapticneurone getssignal next action potenti
0
Paracrine donotcontactbutshort distancetravelthrough
mediatortraveltoreceptor
passivediffusion
canbeextremelyfastandtightlycoupledtoCa

e.gautocrine local 110 potential
unreliablebecause 1transmission action

0
Synaptic useneurotransmitter longdistancetravelbyaxonHast

Electrophysiology studyofsynapse transmission
genetics revolutioninthestudymembranewilldepolarised
0

Endocrine usehormonegoingtoblood streamtotargetan ow


opto
tff
by
treatepilepsybydrugaffectingSV 2A glutamatereceptor
nal

transduction GDP Hi ATP treatdepressionbyblockingreabsorptionofserotonin

eceptor effector
Myasthenia Graviscause bodyproducingits

involveGtpfaonfediffenrydrophinic gyps
CHS'AMP block
by ownantibodywhic

cellsurfacereceptor hydrophilicmoleculesocannot enter thereceptorso patients suffer from musclecontract
impaired
za relateddiseases
Intracellular
pmsoattachtoreceptorinstead
receptor o
smallhydrophobiccrossonand to ftp.kffgeinhgrerjs synapseformationtransmission
attach

gnalusuallyamplify
f intrareceptor exgeneexpression dopaminereleasesynapticvesicleendocytosis
ATPYtifoate
e Epinephrine Gprotein
g s Glycogen Glucose look
fast Alterfunction
slow altergeneDNA
Somedifferent
signal
producesameresponse

Samesignal

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