Term
|
Definition
| Heat Shock Proteins keep cytosolic mitochondrial proteins unfolded until they arrive at the kingdom of mitochondria / Once in the walls, it helps fold the protein |
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Term
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Definition
| Binds to the Matrix Targeting Sequence on the N' end of matrix bound proteins / TOM = Translocase of the Outer Mitochondrial membrane... brings proteins to Gereral Import Pore, which gets it through the outer membrane |
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Term
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Definition
| Translocase of the Inner Mitochondrial membrane / TIM44 and Hsc70 pull the proteins into the matrix |
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Term
| "Path A" Mitochondrial Inner Membrane Targeting |
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Definition
| Protein contains Matrix-Targeting sequence and hydrophobic Stop Transfer Sequence / Zips through Tom40 and then the Stop Sequence stops transfer through the inner membrane and the Matrix signal is snipped. |
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Term
| "Path B" Mitochondrial Inner Membrane Targeting |
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Definition
| Protein contains Matrix-Targeting sequence and an Oxal-Targeting sequence / The protein goes through both membranes before the Oxa1 protein in the inner membrane grabs it and sticks it back twice into the inner leaflet |
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Term
| "Path C" Mitochondrial Inner Membrane Targeting |
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Definition
| Protein contains Matrix-Targeting sequence and multiple internal targeting sequences / Tim9/10 then prevents folding in intermembrane space and aid in multiple passes |
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Term
| Outer Mitochondrial Membrane Targeting |
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Definition
| Proteins possess Outer Membrane Targeting and Stop Transfer Sequence, which interacts with the Tom40 GIP / Not fully understood |
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Term
| What kind of proteins would have a SKL tag? |
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Definition
| Proteins to be sacrificed to the insatiable Peroxisome / PTS1 and PTS2 Peroxisome Targeting Sequence / It is NOT cleaved in the peroxisome |
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Term
| Where are you going to find the SKL tag? |
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Definition
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Term
| What is going on in that Peroxisome? |
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Definition
| Oxidizes the nasties and the fatties, making H202 / Catalase then takes care of the H2O2 / Peroxisomes can divide and form de novo |
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Term
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Definition
| Binds to PTS1 on peroxisome protein, with is ALREADY FOLDED / Pex5 brings complex to Pex14 on the peroxisome |
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Term
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Definition
| Co-transports the ENTIRE Pex5/protein complex into the peroxisome and spits Pex5 back into the cytosol telling it to get back to fucking work |
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Term
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Definition
| Peroxisome de Novo Synthesis: Insert into ER membrane / Mediate Pex19 into ER membrane / w Pex19 promotes insertion of PMP70 (making a Peroxisomal ghost!!!!), Pex2/10/12, and Pex14 --> Can accept new proteins |
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Term
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Definition
| Peroxisome de Novo Synthesis: Once in ER membrane promotes budding / w Pex3 and 16 promotes insertion of PMP70 (making a Peroxisomal ghost!!!!), Pex2/10/12, and Pex14 --> Can accept new proteins |
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Term
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Definition
| Facilitates Peroxisomal division |
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Term
| What proteins would have a Nuclear Localization Sequence (NLS)? |
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Definition
| Ones going TO the nucleussssssss. |
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Term
| What proteins would have Nuclear Export Sequence (NES)? |
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Definition
| Ones LEAVING the nucleusssssss. |
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Term
| Riddle me this? What is the NPC? |
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Definition
| The nuclear pore complex / Made up of nucleoporins / Intermediate filaments extend into cytoplasm / Nuclear basket in nucleoplasm / Ions and small (20-40 kDa) molecules can get through |
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Term
| Goddess, sing to me of the NLS? |
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Definition
| Nuclear Localization Sequence: Rich in basic amino acids (PKKKRKV) / REQUIRES Ran (GTP binding) and Importin to work |
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Term
|
Definition
| Nuclear localization protein: GTP binding protein (monomeric G protein) / Active with GTP bound / GEF mediates the exchange of GDP and GTP (activating Ran) / GAP hydrolysis GTP to GDP (inactivates Ran) |
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Term
| Nuclear Import Mechanism (Getting Cargo into Nucleus) |
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Definition
| Cargo protein with NLS binds to Importin / Nucleoporins aid in PASSIVE diffusion into nucleus w/ Ran-GDP co-transport |
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Term
| Nuclear Import Mechanism (Getting Import Proteins back into Cytoplasm) |
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Definition
| Ran-GDP interacts with GEF and GDP is replace with GTP (active Ran) / Ran-GTP has high affinity for Importin, ergo disassociation of cargo from Importin / The Ran-GTP-Importin difuses thru NPC into cytosol |
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Term
| Nuclear Import (The Return of the Ran-GDP) |
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Definition
| Ran-GTP-Importin interacts with GAP, which hydrolyses the GTP to GDP / Low affinity for Ran-GDP and importin (ergo dissociation)... back to the beginning or end or middle... there are no beginnings or end in circles |
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Term
| What kind of transport is Nuclear Import? |
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Definition
| It is passive--> We are always following concentration gradients. The hydrolysis of GTP causes conformational changes and affinities for Cargo and Importin... this is PASSIVE, PASSIVE, PASSIVE. |
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Term
| Nuclear Import: Concentration gradients of Ran-GTP/GAP, via GEF and GAP |
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Definition
| Inside of the nucleus Concentrations of Ran-GDP-Cargo is low due to GEF, thus in cytoplasm, it wants in / GAP activity in cytosol is high, thus very little Ran-GTP-Importin in cytosol is very low. It moves quickly out of the nucleus |
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Term
| What kind of proteins will have a NES? |
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Definition
| Only the lucky ones... I always wanted an NES. Nuclear Export Signal: The ones going bye bye out of nucleus / It is leucine rich |
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Term
| Ran Dependent Nuclear Export (Getting Cargo out of the nucleus) |
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Definition
| GEF changes Ran-GDP to Ran-GTP / Ran-GTP has a high affinity for Exportin-Cargo(con NES) complexes / This Ran-GTP-Exportin-Cargo complex diffuses out of nucleus |
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Term
| Ran Dependent Nuclear Export (Getting the export machinery back into the nucleus) |
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Definition
| GAP changes Ran-GTP to Ran-GDP, which has a low affinity to exportin / They dissociate / Ran-GDP and Exportin passively diffuse back into the nucleus |
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Term
| Ran-Independent mRNA Export |
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Definition
| Exporters Nxt1 and TAP associate with mRNP and the NPC and aid in diffusion |
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Term
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Definition
| A helicase that unwinds mRNA's secondary structure and removes exporting proteins |
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Term
| How do TAP, Nxt1, and Dbp5 get back into the nucleus |
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Definition
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Term
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Definition
| Causes Lactic acidosis / Problem with E1 subunit (which ends up in the mitochondria) located on chromosome Xp22.1 / Arginine to Proline mutation screws up the matrix targeting sequence) Prevents conversion of pyruvate to Acetyl-CoA / Causes CSF problems |
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Term
|
Definition
| Mutation in the mitochondrial sequence of methymalonyl-CoA mutaase prevents translocation into mitochondria |
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Term
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Definition
| Cryptic mitochondrial targeting sequence --> peroxisomal enzyme, alanine:glyoxylate aminotransferase, into mitochondria whatever the fuck that means! |
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Term
| What are microtubules good for? |
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Definition
| 1. Separate sister chromatids during mitosis 2. Arrange cellular organelles during interphase 3. Tracts for movement 4. Flagella and cilia |
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Term
| Composition of microtubules: |
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Definition
| Linear repeats of alpha and beta heterodimers |
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Term
| What nucelotide triphosphate is on microtubule monomers? And what does it do? |
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Definition
| GTP. On the alpha monomer, it remains GTP. On the beta it is hydrolysed. |
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Term
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Definition
| Stabilizes microtubules. Abrogates mitosis. Cancer killer. |
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Term
|
Definition
| A line of microtubule heterodimers |
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Term
| How many protofiliments does it take to make a microtubule? |
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Definition
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|
Term
| What will find a the negative end of a microtubule? |
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Definition
|
|
Term
| What will find a the positive end of a microtubule? |
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Definition
|
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Term
|
Definition
| 13 protofiliments / Used in interphase and mitosis |
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Term
|
Definition
| 13 and 10 protofiliments / Cilia and flagella |
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Term
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Definition
| 13, 10, and 9 protofiliments / Basal bodies and centrioles |
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Term
| Critical concentration of microtubule dimers |
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Definition
| The concentration of heterodimers needed for them to spontaneously polymerize / The concentration of heterodimers will not exceed the Cc |
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Term
| Microtubule assembly kinetics and polarity |
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Definition
| (+) side has low Cc / (-) side has high Cc / Assembly occurs more quickly at (+) / (+) side usually the "assembly end" while the (-) end is usually the depolymerization end |
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Term
|
Definition
| Most beta tubulin is GTP bound on the (+) side and all beta tubulin that is added must be GTP bound / It begins to get push backwards (treadmilling) and eventually hydrolyses the GTP to GDP, which makes the tubulin less stable at the (-) side. |
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Term
| The GTP-bound dimer pool is high. What is going to happen? |
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Definition
| polymerization at (+) end / Forms a GTP cap (very stable with GTP bound B tubulin concentrations are above Cc, and very unstable when below Cc) |
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Term
|
Definition
| GTP cap is in a solution under the Cc for GTP bound B tubulin / Rapid depolymerization |
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Term
| Three Microtubule Associated Proteins (MAPs) and what they do and how they do it |
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Definition
| Tau, MAP2, MAP4 / Stabilize / They contain lots of + charged AA, which bind to - charged AA on tubulin, neutralizing the charge repulsion between tubulin subunits |
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Term
|
Definition
| Negatively charged acidic projection on MAPs that maintain a certain distance between microtubules / Often in neurons |
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Term
| What happens if you phosphorylate a MAP? |
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Definition
| You would knock out the positive charge and emasculate the MAP. It would then cause depolymerization |
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Term
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Definition
| Bind to the (+) side of microtubule, bends protofiliments, promoting catastrophe / ATP hydrolysis is needed to remove dimers |
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Term
|
Definition
| Also known as OP18 / Bind to the (+) side of microtubule, bends protofiliments, promoting catastrophe / Also enhances GTp hydrolysis / Can be inactivated by phosphorylation |
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Term
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Definition
| Can sever or induce breaks in the microtubules, which exposes GDP bound B tubulin monomers... AH! CATASTROPHE! HEAD FOR THE HILLS!! |
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Term
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Definition
| Drug / Binds tubulin dimers and sequesters them / Lowers dimer concentration (thus more dimers are needed to reach Cc) / Used to reduce WBC migration and inflammation in Gout |
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Term
|
Definition
| Drug / Binds tubulin dimers and sequesters them / Lowers dimer concentration (thus more dimers are needed to reach Cc) / Used to treat Nonhogkins lymphoma, lung, breast, testicular cancers |
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Term
|
Definition
| Drug / Binds tubulin dimers and sequesters them / Lowers dimer concentration (thus more dimers are needed to reach Cc) / Used treat lymphomas, lung and genital cancers, and HPV genital warts |
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Term
|
Definition
| Synthetic drug that prevents spinal assembly during mitosis / Arrest in G2 cell cycle phase / Used to synchronize cells in culture |
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Term
| Alzheimer's and microtubules |
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Definition
| Improper phosphorylation of Tau proteins / Destabilizes microtubules |
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Term
|
Definition
| Proline isomerase converts spontaneously formed proline cis isomers back to trans. This drives dephosphorylation of APP and Tau and the microtubules remain sound. Defective Pin1 will causes more cis proline isomers on Tau and APP, which will then be phosphoylated, which will then causes depolymerization of microtubules in brain, which will cause amyloid plaques and neurofibrillary tangles, which will cause Alzheimer's Disease. |
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Term
|
Definition
| Made from actin, which is made by the intertwining of two thin filaments / Can polymerize and depolymerize / Muscle contraction, cell adhesion, motility, and stabilization of microvilli / The smallest |
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Term
|
Definition
| Mechanical integrity of the cell, motility, and serves as scaffolds for signaling molecules / No polymerization and depolymerization / stiff |
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Term
| Duchenne Muscular Dystrophy and actin |
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Definition
| Dystrophin links the actin cytoskeleton to the extracellular matrix / Dystrophin binds the protein alpha/beta Dystroglycan in the plasma membrane / On the other side of the membrane, there are extra cellular matrix proteins like laminin, agrin, and perlecan that bind to carbohydrates on the alpha/Beta Dystroglycan / Muscle contraction needs dystrophin to stabilize the interaction between the cytoskeleton and the extracellular matrix / Without dystrophin, the extracellular proteins will tear the plasma membrane, causing destruction of muscle cells / Fibroblast cells migrate to site and create nonfunctional scar tissue |
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Term
|
Definition
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Term
|
Definition
|
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Term
|
Definition
| With Actin, gives red blood cell there biconcave shape |
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Term
| What is required for actin polymerization? |
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Definition
|
|
Term
| What is the (-) end of G-actin? |
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Definition
| Where the ATP-binding cleft is exposed to the surface |
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|
Term
| What is the (+) end of G-actin? |
|
Definition
| Opposite where the ATP-binding cleft is exposed to the surface |
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Term
| Explain actin polymerization |
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Definition
| A (+) and (-) G-actin end bind together to make F-actin |
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Term
|
Definition
| Binds to F-actin with ADP containing subunits and breaks them, speeding up depolymerization |
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Term
|
Definition
| Enhances the exchange of ADP to ATP on G-actin / This is needed if the G-actin will be used again |
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Term
|
Definition
| Binds to to ATP-G-actin and sequesters it or releases it to keep a constant concentration: This helps keep a constant pool of ATP-G-actin |
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Term
|
Definition
| Binds to (+) end of F-actin and prevents addition of new ATP-G-actin monomers |
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Term
|
Definition
| Binds to (-) end of F-actin and stabilizes it |
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Term
|
Definition
| Stimulate the assembly of of long unbranched F-actin. These fibers are found in stress fibers and contractile rings. |
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Term
|
Definition
| Stimulates the formation of branched filaments, which are found in the leading edge of migrating cell / Controlled by signal transduction |
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Term
|
Definition
| Cause cell migration / Very often growth factors that bind receptors on migrating cells, setting up a signalling cascade |
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Term
| Steps of mammalian cell migration |
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Definition
| Step 1: The extension of the plasma membrane to form lamellipodium via increasing the length of actin filaments / Step 2: Adhesion of lamelliodium / Step 3: Translocation - bulk of cell moves toward adhesion point / Step 4: Adhesion point in back is broken, via pulling by F-actin. Membrane proteins are recycled |
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Term
|
Definition
| cross linked parallel F-actin in intestinal microvilli / Fibrin stabilizes these structures |
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Term
|
Definition
| Organizes F-actin of the stree fibers during migration / Also muscle contraction |
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Term
|
Definition
| Cross links and organizes F actin into a meshwork network just under the plasma membrane / It is a long fibrous molecule that forms the cross linking with F actin / Supports plasma membrane |
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Term
|
Definition
| Cross link the cytoskeletal proteins to extracellular matrix / Transmembrane proteins / This fixes cells to their tissues |
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Term
|
Definition
| Has weak RBCs due to a defect spectrin, protein 4.1, or ankyrin / Patients usually have anemia and/or large spleens or gallstones with excess amounts of heme. |
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Term
|
Definition
| Found in epithelial cells / Tissue strength and integrity |
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Term
|
Definition
| Found is muscle, glial, and mesenchymal cells / Sarcomere organization and integrity |
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Term
|
Definition
| Found in neurons / Axon organization |
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Term
|
Definition
| Found in nucleus / Nuclear structure and organization |
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Term
| Epidermolysis bullosa simplex |
|
Definition
| Problem with keratin IFs / Blisters form very easily |
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Term
| Type I OI (Osteogenesis Imperfecta) |
|
Definition
| Also called brittle bone disease - problems with collagen production - Could be a change for larger AA instead of the usual Gly |
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Term
|
Definition
| Child dies at birth due to collapsed |
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Term
|
Definition
| Used to treat Osteogenesis Imperfecta - it inactivate and destroy osteoclast - they also decrease the destruction of osteoblasts |
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Term
|
Definition
| Three collagen chains coiled into a left handed alpha triple helix |
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|
Term
| Collagen consensus sequence |
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Definition
| Gly-X-Y / X and Y are endo-proline and exo-hydroxyproline / right handed helix breakers |
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Term
|
Definition
| Tropocollagen - H-bonds between strands - Gly make steric hendernce not a problem |
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Term
|
Definition
| Collagen (high tensile strength, low elongation, in tendons) / Elastin (low tensile strength, high elongation, in skin) |
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Term
|
Definition
| Deficiency of vitamin C, which is an cofactor needed to turn proline to hydroxyproline / Thus, the collagen that is made falls apart very easily |
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|
Term
| What enzyme is responsible for the hydroxylation of proline? |
|
Definition
|
|
Term
| Mechanism of 4 Prolyl-hydroxylase |
|
Definition
| Uses molecular oxygen to hydroxylate proline and turns alphaketoglutarate to succinate / USED IRON AS COFFACTOR / Vit C is oxydized needed to keep iron reduced to ferrous iron |
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|
Term
| Where in the cell does collagen biosynthesis take place? |
|
Definition
| Rough endoplasmic reticulum... it is then translocated into ER. |
|
|
Term
| Collagen biosynthesis traslocation into the ER... |
|
Definition
| Conversion of proline to hydroxyproline |
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|
Term
| Collagen biosynthesis once in the ER... |
|
Definition
| Translocation signal is cleaved, creates PRO-COLLAGEN |
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|
Term
| Creation of collagen triple helix... |
|
Definition
| Done by a creation of disulfide bonds between strands on C' ends and the triple helix / Procollagen is then secreted out to ECM where N' and C' ends are cleaved and mature collagen is formed |
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|
Term
| ECM triple helix processing |
|
Definition
| Five collagen fibers cross linking to higher order |
|
|
Term
| How to higher order collagen fibers form in the ECM? |
|
Definition
| The enzyme Lysyl oxidase processes the cross linking / It uses Cu2+ |
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Term
|
Definition
| Lysyl oxidase or Cu2+ / Kinky, steeled colored hair, growth problems |
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Term
|
Definition
| Deficincey in the ECM Procollagen peptidase / The C' and N' end are not cleaved, hence loose collagen |
|
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Term
|
Definition
| Most abundant collagen - most connective tissue |
|
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Term
|
Definition
| Cartilage and vitreous humor |
|
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Term
|
Definition
| Extensible connective tissue (eg skin, lungs, blood vessels. |
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Term
|
Definition
| Tissues containing type I |
|
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Term
|
Definition
| Fibril associated / Tissues containing type I collagen |
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Term
|
Definition
| Network forming / Basal lamina |
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Term
|
Definition
| Anchoring filament / Attachments of the basal laminae to underlying connective tissue |
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Term
|
Definition
| Hydrophobic / Rich in G,A,V,P,K / Few hydroxylated AA / deaminated lysines cause cross linking |
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|
Term
|
Definition
| Mutation in fibrillin gene / Impaired elastin function / Long slender limbs / Heart problems |
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Term
|
Definition
| Expressed in neutrophils and normally degraded in ECM / Alpha-1-antitrysin helps regulate this / Bad A1-AT builds up and causes damage to the liver / Too much elastase and not enough elasin to degrade causes lung degradation |
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