ANAT212

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Created by:

ggasperlin  on April 17, 2012

Subjects:

McGill Anatomy

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Anat212

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ANAT212

Acetyl CoA
acetyl group attached to Coenzyme A by a high energy thioester bond
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Acetyl CoA acetyl group attached to Coenzyme A by a high energy thioester bond
fructose-1,6-biphosphate end product of energy investment to glucose (bumble bee futile cycle)
PFK (phosphofructokinase) enzyme that transfers phosphate onto glucose-6-phosphate. allosterically regulated by ADP/AMP
glyceraldehyde-3-phosphate forms a temporary covalent bond with enzyme through a thiol group, enzyme reduces NAD to NADH, leaves a high energy anhydride bond
1,3-biphosphoglycerate high energy anhydride bond is displaced by inorganic phosphate to create ATP
phosphoenolpyruvate high energy enol phosphate linkage is transferred to create ATP
creatine phosphate small molecule with extremely rapid energy source
pyruvate end point of glycolysis, acid that is damaging to cells so has to be changed
citrate combination of acetyl CoA and oxaloacetate, start of krebs cycle
oxaloacetate 4 carbon molecule that is not consumed in the krebs cycle
porins transport pore in OM of mitochondria allowing anything < 5kDa through
cardiolipin lipid in the IM of mitochondria making it impermeable
NADH dehydrogenase complex removes electrons from NADH and captures as packets of energy, pumps a proton from the matrix to IMS
Ubiquinone small hydrophobic molecule that moves electrons between NADH dehydrogenase complex and the cytochrome b-c1 complex
cytochrome b-c1 complex passes electron to cytochrome C, moves proton into IMS
cytochrome C carries electrons to the cytochrome oxidase complex
cytochrome oxidase complex reduces oxygen, accepts electrons one at a time but passes them on four at a time, transports a proton to IMS for each
heme group (porphyrin) involved in transporting electrons in the transport chain, can have iron-sulfur or copper centre
F0F1 ATP synthetase synthesizes ATP in mitochondria by oxidative phosphorylation when turned by import of proton
CLK-1 involved in biosynthesis of ubiquinone
EGF, PDGF, TGFa growth factors ineuce proliferation of fibroblasts and keratinocytes
TGFb inhibit keratinocyte proliferation
FGF growth factor inducing proliferation but also promotes angiogenesis
MMP matrix metalloproteases, remove scar tissues
estradiol, testosterone, vitaim D2 liposoluble steroid hormones localized in the cytoplasm or nucleus that act to directly regulate gene expression
g-protein linked receptor largest family of cell surface receptor, has 7 TM regions
Src tyrosine kinase doesn't have an extracellular domain, binds to itself via the SH2 region and phosphorylated T-527
SH2 100 amino acids, binds to phosphorylated tyrosines, binding site for amino acid side chain shows specificity
SH3 50 amino acids, binds to proline rich residues X-P-P-PX-P
PLCg binds directly to phosphorylated RTK, gets phosphorlyated and activated
p85 induces conformational change in p110 by approaching phosphorlyated RTK and pushing p110 against the membrane
Grb2-Sos-Ras changes into a GNRF which activates Raf
Ras GTPase activated by GEF, deactivated by GAP
oncogene dominant cancer causing gene
tumor suppressor gene recessive cancer causing gene
forci countable piles of cells growing in a multilayer
E6 E3 Ub-ligase that degrades p53 in HPV
E7 binds to Rb and inhibits it in HPV
MLH1 tumor suppressor gene that doesn't get mutated just turned off
Abl-Bcr active tyrosine kinase in CML, fused protein from chromosomes 9 and 22, causes WBC to proliferate, blocked with Gleevec
HIF accumulation of this in hypoxic conditions induces transcription genes that attract blood vessels
VEGF makes blood vessels grow and proliferate towards tissues low in oxygen
bicoid early classical example of a morphogen
eve skips the even numbered stage in embryo patterning
ftz not enough segments in embryo patterning
Wnt binds to frizzled in the canonical pathway
GSK3b/Axin/APC/CKIa complex formed with beta-catenin
beta-catenin when it accumulates it enters the nucleus and binds to TCF to turn on target genes, can be mutated in many cancers
groucho negative regulator of transcription displaced by beta catenin
pax2 transcription factor found in the kidneys, if you don't have it you don't have kidneys, similar to pax8
gata3 downstream of pax2, zinc-finger transcription factor, responsible for HDR syndrome
GDNF morphogen expressed in and secreted from the mesenchyme, induces ureter generation
Ret/GFRa1 GDNF's receptor in the epithelium
spry1 inhibits Ret/GFRa1
LAR family essential to ureter maturation
RPTP member of the LAR family, receptor protein tyrosine phosphatase (opposite of RTK)
CDK (Cyclin Dependent Kinase) becomes active when bound to a cyclin
Cyclin regulates CDKs and their kinase activity
G1/S (Cyclin) shoots up to initiate the cell cycle, but immediately drops before S-phase
S (Cyclin) synthesized while G1/S cyclin performs its cycle; present from S-Phase to M-Phase
M (Cyclin) helps in the division processs of the cell into two daughter cells
CAK (Cdk-Activating Kinase) phosphorylates the active site loop of a cyclin-CDK complex, causing a slight conformational change and activating the entire complex; need this for a FULLY ACTIVE cyclin-Cdk complex
Wee1 Kinase; places on inhibitory phosphate on M-Cdk; inactivates M-Cdk
Cdc25 Phosphatase; removes the inhibitory phosphate placed on M-Cdk by Wee1; activates M-Cdk; positive feedback by M-cyclin
p27 binds to the Cyclin-Cdk complex and holds it in a conformation rendering the complex inactive; similar to p16 and p57
p16 tumor suppressor gene; usually binds the G1/S-cylin-Cdk complex; loss of which results in tumor
Ubiquitin specific signal found on the target substrate that sends the target substrate to the proteasome for degradation
SCF complex responsible for signalling the degradation of the CKI
F-box confers specificity in the SCF complex
Skp and Cullin form the backbone of the SCF complex
CKI (CDK Inhibitor Protein) destroyed in the cell cycle by proteasome; needs to be phosphorylated by a cyclin-Cdk complex in order to be targeted for degradation
APC (Anaphase Promoting Complex) responsible for the degradation of M-cyclin; poly-Ub the M-cyclin/Cdk complex
Cdc20 activates the inactive APC; initiates M-cyclin degradation
ORC (Origin Recognition Complex) binds to Origins of Replication and marks the start of DNA replication
Cdc6 binds to the ORC in G1 forcing a conformational change and attracting Mcm proteins
Mcm proteins that make a ring-like structure around the DNA at a DNA replication start site; contain DNA helicases
Pre-Replicative Complex Mcm + ORC + Cdc6
S (Cyclin) phosphorylates the Cdc6 triggering DNA Synthesis; Cdc6 dissociates and gets degraded leaving ORC to get phosphorylated and inactive
phosphorylation of ORC prevents the Mcm complex from assembling, keeps Cdc6 from binding, and turns the whole system of DNA Synthesis off; prevents re-replication
APC E3 Ligase that promotes proteolysis of M-cyclin
APC clips the cohesins and condensins and targets them for degradation
cdc20 binds the APC and activates it
APC poly-Ub securin signalling it for degradation
securin inhibitory protein for separase protease
M-cdk stimulates cdc20-APC activity triggering degradation of M-cyclin
Hct1-APC inactivated by M-cdk and activated when [M-cdk] low
M-cdk inactivated by Hct1 or Sic1 and activated when [Hct1] or [Sic1] low
Sic1 cyclin dependent kinase inhibitor (CKI) like p27; degraded when phosphorylated; degrades m-cyclin
Hct1 activates APC to degrade M-cyclin
p21 suppresses G1/S Cdk and S Cdk activities following DNA damage; activated by active p53
p53 activates p21 in response to DNA Damage
ATM/ATR kinase phosphorylates Chk1/2 in response to DNA damage
Chk1/2 phosphorylates p53 in response to DNA damage
Mdm2 poly-Ub p53
MAP Kinase goes to nucleus and phosphorylates the transcription factor Myc
Myc activates G1 cdk; how cells in G1 or G0 get back into the cell cycle; excess leads to permanently active p53
RB keeps E2F in an inactive form; dissociates when phosphorylated
E2F transcription factor with positive feedback on itself; kept inactive by RB
Arf result of excess Myc; binds to and inhibits Mdm2 therefore activates p53
cdc25 inhibited by damaged or unreplicated DNA
Rapamycin analogs are used to treat some cancers
Aflatoxin B1 when metabolized by the liver, becomes a reactive compound capable of making the DNA adduct and cause a break in the normal transcription
Shh secreted from the notocord and sent to the floorplate
Ptch1 cell surface receptor that represses Smo
Gli3 binds to DNA and prevents accumulation of target genes; acts as a repressor in the Shh pathway
Shh binds and represses Ptch1
Smo activates Gli1, Gli2, and Gli3
Cyclopamine natural inhibitor of the Shh Signalling pathway; acts as a repressor of Smo
BMP (Bone Morphogenic Proteins) secreted from the roof plate, opposite Shh; generates the far of dorsal neurons in response to different concentrations of BMP
Ubx when overexpressed, drosophila loses its wings
Ubx when mutant; second pair of full wings instead of haleteres
Notch membrane bound receptor that is activated by Delta; represses cell specialization; Stronger Delta, Weaker Notch = specialized cell
Delta activates Notch
TACE cuts Notch on the outside of the plasma membrane
(g)Secretase cuts Notch on the inside of the plasma membrane
Intracellular Domain of Notch after the 2nd cut by gamma secratase, set free to complex wtih another protein, translocate to the nucleus, and bind CSL transcriptioin factor
Notch displaces co-repressor on CLS and brings in a co-activator protein that activates transcription
Numb repressor of Notch signalling; prevents Notch from entering the nucleus; cells that inherit it will never activate Notch
Numb determinant involved in the assymetric division of cells present on one side of the cell BEFORE cytokinesis
Numb allows for differentiation between cells because there is a repressor in one of the cells that prevents certain genes from being activated;
DIX and PDZ activation by canonical Wnt pathway leads to gene transcription and nothing else
DEP and DIX and PDZ activation by non-canonical Wnt pathway leads to planar cell polarity
kit needed for the survival of neural crest-derived pigmentation cells; lack of which prodcues a mild mutation such as a white spot on the forehead fur to cell death
netrin component of the floor plate that spinal cord cells grow towards; causes axon to cross the midline once
Slit and Semaphorin repellants expressed at the midlin that bind receptor Roundabout(Robo) on the axon and ensure that the nerve turns away from midline and goes to the brain

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