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87 Cards in this Set
- Front
- Back
3 kinds of protein filaments |
Intermediate Microtubules Actin |
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What are the different filaments composed of? |
Intermediate: various fibrous proteins Microtubules: tubulin Actin: actin |
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Intermediate filaments |
Rope like, strong, provides mechanical strength to cells to withstand stress |
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Where are intermediate filaments |
A network in the cytoplasm, around the nucleus and radiating out In the nucleus as a meshwork called the nuclear lamina under the inner membrane of the envelope |
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Desmosomes |
Cables connecting intermediate filaments between cells in tissues to increase structure strength |
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Epidermolysis bullosa simplex (EBS) |
Rare mutation that prevents proper keratin filament assembly |
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Structure of intermediate filaments |
Ropes made of multiple stands that are made of filament proteins. All proteins have N-terminus globular head, C-terminus globular tail, with an alpha helical region connecting them |
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Subunits of intermediate filaments |
2 protein units wind as a coiled coil. 2 coils line up head to tail as tetramer. Tetramers line up end to end as protofilaments. 8 protofilaments wind together to form intermediate filament |
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Intermediate filament assembly/breakdown |
Regulated by phosphorylation of the filament proteins |
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Microtubules |
Long, cylindrical, hollow rods, made of tubulin, help determine cell shape, provide tracks for vesicle movement, positioning of organelles, separation of chromosomes during cell division |
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Where are microtubules |
Animal cells: originate from the centrosome and extend out |
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Subunits of microtubules |
Tubulin subunit with an alpha and beta unit, Chains of tubulin alternating alpha and beta form protofilaments (one end is beta +, the other is alpha -), 13 protofilaments around holow core make microtubule |
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Centrosomes |
Initiation of microtubulal assembly, - end attaches to gamma tubulins in centrosome |
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Dynamic instability |
Alternating building and breakdown of microtubules quickly to allow remodeling of the cytoskeleton as needed |
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Microtubule associated proteins |
MAPs proteins that help stabilize microtubules, the interactions give the cell shape and organization |
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Antimitotics |
Drugs that fight cancer by preventing cell division through stopping assemby/breakdown of microtubules |
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Motor proteins |
Kinesins and dyneins. Attach to cargo to pull along microtubule track. Nrg provided by ATP. Also keep organelles correctly positioned Kinesins: towards + Dyneins: towards - |
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Actin filaments |
Most abundant, long fibers, cell movement, phagocyctosis, cell division, cell shape, intracellular traffic, muscle contraction |
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Subunits of actin filaments |
Globular proteins, 3 bind as trimer, have plus and minus end, form similar to microtubules |
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Where are actin filaments |
Just inside plasma membrane as the cell cortex |
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Cell movement |
Actin network changes shape by growing, making protrusions that help the cell crawl/perform phagocytosis |
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Signal transduction |
The transformation of info in the signal from one form to another |
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Signals that cross the cell membrane |
Small, hydrophobic, steroid hormones (lipid molecules), bound by receptors inside cell |
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What happens when a steroid binds it's receptor? |
The receptors are dormant transcriptional activator that bind to enhancers and cause transcription once bound |
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Stages of interphase |
G1: growth phase 1 S: DNA synthesis G2: growth phase 2 |
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When do cells decide to divide? |
Late G1. If they don't want to divide they drop out into the G0 nondividing state. This point is called START |
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When do cells decide to divide? |
Late G1. If they don't want to divide they drop out into the G0 nondividing state. This point is called START |
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Factors influencing cell division |
Is there sufficient food for new cells, is there the signal, how crowded is it |
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Cell checkpoints |
Mechanisms that allow the cell to proceed from one stage to another only after the previous one is confirmed as completed correctly |
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Controlling cell cycle progression |
Controlled by special protein kinases called Cdks, cyclin dependent kinases, that must be bound to a cyclin protein to be active |
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What happens to the cyclin after the cdk does its job |
It is sent out of the nucleus and destroyed |
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Factors that regulate cdk activity |
Phosphorylation on 1 binding site, none on the other 2 Cdk inhibitors: bind to Cdk to inactive thrm |
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What happens if a cell has damaged dna |
Levels of the transcriptional protein p53 increase, increasing gene expression of p21. P21, a Cdk inhibitor, binds the S-Cdk and stops it from entering S phase until the damage is fixed |
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What if the damaged dna can't be fixed |
P53 triggers cell death |
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How is DNA only copied once |
Licensing factors: proteins that bind near origins of replication only during G1. They allow the initiation of replication. Once replication is started the factors are removed from the nucleus |
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M-Cdk/MPF |
Kinase that starts mitosis Cytoplasm of cell in M sent interphase cells into M. Each proteins was tested until the correct one was isolated Cdk 1: constant throughout cycle cyclin B: high only before/during mitosis |
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How does M-Cdk work |
Transfers phosphate from ATP to target proteins which activates cell pathways, triggering many of the events in mitosis |
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Prophase |
Chromosomes condense when Condensins are phosphorylated by M-Cdk |
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Prometaphase |
Nucleur envelope breaks down when M-Cdk phosphorylates lamins (lamina proteins) |
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Metaphase |
Mitotic spindle forms when M-Cdk causes the phosphorylation of microtubule associated proteins. This stabilizes the microtubules so they can attach to the kinetochores of the chromosomes and align them at the metaphase plate |
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Anaphase |
The breakdown of regulatory proteins triggers the separation of the Chromosomes |
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APC |
Anaphase promoting complex, adds ubiquitin to regulatory proteins to start anaphase. |
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Securin and the cyclin component of M-Cdk |
Ddgradated by APC Securin: releases separase, which breaks the cohesins between sister chromotids Cyclin of M-Cdk: lowering the level starts the cell back to interphase and triggers cytokinesis |
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Cytokinesis |
Animal: Contractor ring of actin and myosin pinch the cell in 2 Plant: formation of a cell plate |
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Common stem cell properties |
Not differentiated Potential to divide indefinitely Can undergo differentiation |
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Pluripotent |
Stem cells that have the potential to differentiate into many different kinds of cells |
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Blastocyst |
About 100 cells, has 3 structures 1. Tropoblast, surrounding cell layer 2. Blastocel, a hollow cavity 3. Inner cell mass, the group of cells that develop into the embryo proper |
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Somatic cell nuclear transfer |
Nucleus of somatic cell used to trick oocyte into seeming fertilized and developing. Matches cells to patient |
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Induced pluripotent stem cells |
Inducing adult differentiated cells to express key genes of embryonic cells |
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Apoptosis |
Programmed cell death, a built in cellular process by which cells die via a regulated series of changes within the cell |
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Why are cells programmed to die? |
1. To give form to developing embryos 2. To maintain adult tissues in balance 3. To eliminate cells that might be infected 4. To get rid of cells with lots of dna damage |
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What happens in cell death? |
Cell sheinks, cytoskeleton collapses, nuclear envelope breaks down, DNA fragments. Cell surface signals apoptosis and it's phagocytosed by a healthy neighbor cell for recycling |
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Caspases |
Enzymes that carry out apoptosis |
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What signals apoptosis |
Can be internal, such as p53 causing death when the DNA is too damaged External through cell death signals |
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How are caspases activated |
Inactive precursors are converted to the active form by being cut by protease. Once active, the caspases can cut other precursors... caspase cascade |
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Protecting cells from apoptosis |
Cellsurvival signals tell cells to express genes that inhibit apoptosis |
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Metastatis |
The process of tumor cells moving to new places in the body |
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Initiating agents of cancer |
Chemical carcinogens, radiation, viruses... it causes damage and/or mutations that can lead to cancer |
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Cancer cell abnormalities |
Proliferation without growth hormone stimulation Failure to undergo apoptosis Divide indefinitely/reactivate telomerase |
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Oncogenes |
Genes that promote cancer because when they are mutated they can cause cancer |
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Proto-oncogene |
The original unmutated oncogene that is required for functioning Often encode proteins that promote proliferation |
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Ras gene mutations |
Causes mutant ras proteins that can't hydrolyzed GTP so they are stuck on and proliferation follows |
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Tumor suppressor genes |
Normally inhibits cell division, if mutated it allows division abnormally |
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P53 mutations |
Removes break during cell cycle between G1 and S Allows cells with dagamed DNA to divide instead of undergoing apoptosis/repairing damage |
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Why are mutated p53 genes difficult cancers |
Radiation damages DNA to trigger apoptosis, which won't work if p53 isn't working to signal for apoptosis |
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For a cell to divide it must... |
Receive a growth signal Pass the signal to intracellular molecules Activate a cascade of protein kinases Phosphorylate target proteins Tumor suppressor must approve |
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Cancer treatments |
Block growth factors Block growth factor receptors Prevent ras activation P53 targeted drugs |
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P53 cancer drug |
Virus without E1B that disables host p53 has to attack cells already lacking p53, ie cancer cells, which kills the cancer cells |
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Signals that can't cross the plasma membrane use |
Gated ion channels G-protein linked receptors Receptor tyrosine kinase |
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Gated ion channels |
Neutrotransmitters, membrane channels ions travel through, signal binds and opens gate, allowing ion flow |
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G protein linked receptors |
Epinephrine, pass on signal with help of G proteins |
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Structure of G protein receptors |
Polypeptide chain that threads back and forth 7 times through plasma membrane one end is extracellular to bind signal, other end is in the cytosol |
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G proteins |
A protein that can bind GTP/GDP 3 subunits of alpha, beta, and gamma. Alpha binds GTP/GDP Unstimulated: trimeric, GDP Stimulated: GTP, alpha with GTP and beta gamma unit |
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Factors for g protein stimulation length |
How long the alpha and beta gamma units bind to their targets How long the alpha and GTP are associated |
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G proteins for protein kinase A |
Using epinephrine Epinephrine binds to receptor, g protein is activated, alpha subunit activates adenylate enzyme, producing cAMP a second messenger that spreads the signal |
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How does cAMP pass the signal on |
cAMP levels are mediated by protein kinase A which is composed of 2 catalytic and 2 regulatory subunits, high cAMP activates PKA and binds to release the catalytic subunits to phosphorylate other proteins |
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How does cAMP pass the signal on |
cAMP levels are mediated by protein kinase A which is composed of 2 catalytic and 2 regulatory subunits, high cAMP activates PKA and binds to release the catalytic subunits to phosphorylate other proteins |
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What happens to cAMP once it's job is done |
It is broken down by phosphodiedterase |
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G proteins for protein kinase C |
Alpha subunit activates phospholipase C which produces the second messengers IP3 and DAG |
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What does IP3 do |
Diffuses to the ER membrane where it binds to gated calcium ion channels, releases calcium into the cytoplasm from the ER lumen. This activates protein kinase C |
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What does DAG do |
On the plasma membrane, works with calcium to activate PKC. pkc phosphorylates cell proteins |
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Receptor tyrosine kinase |
A cell surface receptor that also has tyrosine kinase activity. Receptor is on cell surface, kinase is on the cytoplasm |
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What happens when RTK binds |
2 receptor molecules dimerize, bringing tails of the receptor together. The tyrosine kinase activity of the tails is activated and they phosphorylate each other's tyrosine... autophosphorylation |
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What does phosphorylating the RTK tails do |
Triggers the assembly of an intracellular signaling complex on the tails. The tyrosine are binding sites for signaling proteins to pass the message on |
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RTK ras activation |
One of the complex proteins interacts with ras and gives it a GTP, activating it the ras triggers a phosphorylation cascade that distribute the signal |
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MAP kinases |
The 3 kinases activated by ras, Mitogen Activated Protein kinases |
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What are the common features of signal transduction pathways |
Receptor Intermediates Target |