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37 Cards in this Set
- Front
- Back
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about 600 mya, euk cells begin losing their __ and gaining __ thus, they needed ___ |
autonomy and gaining specialization signaling/ transduction |
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ligands |
hydrophilic, large, cant cross PM membrane usually |
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epithelial cells are controlled by __ signaling released from__ from __ cells |
paracrine crypt layer housing stem cells which undergo asymmetrical replication |
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signal transduction |
extracellular messages causing a response through a pathway by binding approp receptor |
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signal transduction is |
dependent on concentration levels non covalent and non permanent binding |
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phosphorylation of three main a.acids_ for protein kinases dePed by |
serine threonine tyrosine phosphotases |
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extracellular domain __ layer |
where ligand and receptor bind input |
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transmembrane domain __layer |
catalytic, dimerizes, PO4's things hidden layer |
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cytoplasmic domain __layer |
relays and transduces signal through the cell until the response molecule is reached output layer |
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how many promotors are there in the genome how many do each control what do they lead to the dna sequence |
22,000 promoters each controlling about a couple 100 genes each they direct RNA polymerase |
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PDGF secreted by__ its receptor is ___ and __ respond to PDGF signal PDGF is a __ this is an ex of _ |
platelets secrete Platelet Derived Growth Factor which is bound by PDGF receptor on fibroblast cells. mitogen, which begins migration and proliferation of fibroblasts to wound areas paracrine signaling |
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fibroblast growth is__ theyre found in a __ |
density dependent and contact inhibited confluent monolaye |
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what types of cells do no respond to PDGF and also do they die? |
cells that are mutants in both alleles for the receptor -/- are not able to divide and migrate towards wound areas to recreate a monolayer they are however alive |
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RSV and the src gene both express __ the first of its kind src is __ you can use a __ to visualize its substrates |
tyrosine kinase, TK the wild type protein P's at tyrosines pleiotropic, changes many phenotype pathways polyacyrilmide gel with antibody for P'ed tyrosines |
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EGF and EGFR homologous sequence of ___ to ___ |
epidermal growth factor and its receptor src sequence is homologous to cytoplasmic domain sequence of the EGFR |
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EGRF and src are both __ |
receptor tyrosine kinases RTKs |
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the first identified RTK how many RTKs are there what are they known to function in |
was EGFR approximately 60 in the genome theyre known for euk cell proliferation |
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EGFR aka __ involved in __ cancer caused by ___ in __ cell surfaces |
Her 2 receptor o/e on epithelial cells leading to breast carcinomas and glioblastomas |
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Wild type RTK functioning |
they are monomeric with no ligand and dimerize when ligand binds and they are auto/cross/trans phophorylated |
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an altered EGFR _ leading to__ is sends__ |
erbB receptor protein is truncated and has no amino extracellular domain receptor, therefore it is active independent of ligand and it is o/e mitogenic constitutive signals. |
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ways to get a net plus of receptors |
o/e mutations in sequence amplicons/ deletions deregulated quenching via endocytosis aka low turnover truncation of ectodomain translocations and fusions |
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autocrine |
cell is abnormal and is making and sending its own ligand for the receptors it makes itself. ligand binds receptor. poor prognosis, sometimes more than one loop. |
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Her 2 receptor o/e by how much? o/e found in __% of breast cancers |
up to a million times more than normal receptors found 20-25% of cases |
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herceptin activity |
herceptin is multimodal, it uses antibody and ligand tagging to stop the her 2 receptor activation to tag the cell for immune sys dest and also inhibits the catalytic kinase domain in the cytoplasm from transducing a signal. stops proliferation |
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RTK activity WT |
lig binds receptor, conf change, the P on the tyrosine cellular domain occurs from the receptor itself or another one. |
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RTK activity mutant |
lig doesnt have to bind receptor for Plation. if theres o/e of receptors they transiently dimerize due to lateral movement and thus are able to activate to very low levels of ligand--hypersensitive OR theyre truncated and they can dimerize indep of ligand. |
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example of a mutant RTK additional exs we never went over |
tropomyosin to RTK fusion-- truncated ectodomain the tropomyosin amino terminal is always dimerized so the RTK is active. cooh domain always on leucine zipper- nucleoporin |
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a cytokine receptor pathway |
Jak STAT pathway |
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Jack STAT pathway does __ mechanism__ Jaks are __attached to TKs |
activated transcription factors in nucleus first ligand binds receptor then the Jaks cross P each other, then the Jaks P themselves. Now, the domain binds STATs. the Jaks P the STAT, then the STATs are able to dimerize and enter the nucleus. noncovalently associated with the RTKs |
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Jaks prevalent in __ cells |
hematopoietic cells |
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integrin signaling inner __ domains linked with __ |
integrin receptors bind ECM proteins as their ligands- they are keeping the inside cytoskeleton connected to the outside of the cell. inner cooh domain linked with cytoskeletal proteins- FAK and ras/src and signaling |
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if integrins do not sense the outside ECM proteins then the cell undegoes |
anoikis apoptosis |
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integrin receptors provide cell with loss with ECM means cell is __ and __ |
anchorage, density dependence, monolayer, no migration cell is migrating/deregulated and is neoplastic moving out of its compartment. |
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Ras __ protein it is triggered by |
Ras is a G protein upstream GEF-- guanine nucleotide exchange factor |
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how is ras protein activated |
it is activated by GEF EXCHANGING GDP for GTP. activated ras goes on to have downstream effects |
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how is ras deactivated |
ras is deactivated by GAP-- GTPase activating protein which takes the P off of the/hydrolyzes GTP to make it GDP again, thus deactivating ras. |
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how do ras caused cancers act specifically |
they do not allow GAP to hydrolyze P off of GTP GAP is not allowed to deactivate ras and thus ras stays on. |
