Term
| Life depends on the ability of cells to grow, copy their genetic information, and ____ pass that information onto the next generation. |
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Definition
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Term
| What is the name of the phase that happens when the cell has left the cell cycle? |
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Definition
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Term
| Why are checkpoints in the cell cycle important? |
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Definition
1. Allows the cell to monitor its own progress
2. Allows the controller to respond to extracellular signals from the environment and from other cells. |
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Term
| Once the cell is past the checkpoint... |
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Definition
| it cannot pause the cell cycle. The cell is committed to completing the subsequent step. |
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Term
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Definition
| Cell Division Cycle mutants |
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Term
| One type of mutant phenotype involves an inactivation of some protein involved in activating or pushing the cell cycle forward. What does that mean? |
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Definition
| That you have basically blocked an activator. Meaning that the cell can no longer proceed through the cell cycle. |
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Term
| What kinds of mutants divide early, skipping a normal control point? |
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Definition
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Term
| Wee mutants are expected to be deficient in a product that normally ____ passage through a size checkpoint. |
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Definition
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Term
| How do you identify the mutated gene that is responsible for the observed phenotype? |
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Definition
| add back wild type genes, until you find the one that fixes the mutation |
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Term
| What are the two ways passage through the cell cycle is controlled by? |
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Definition
| Protein phosphorylation (CDKs) and Protein Degradation (Ubiquitin-protein ligases (adding tags)) |
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Term
| The activity of Anaphase-promoting complex (APC/C)is important in pushing the cell through which checkpoint? |
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Definition
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Term
| What is the heart of the cell cycle control system? |
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Definition
| Cyclin-Dependent Kinases (CDKs) |
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Term
| ____ of these kinases (CDKs) rise and fall as the cell progresses through the cycle. |
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Definition
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Term
| Kinase activity is dependent on presence of ____ |
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Definition
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Term
| What are the 3 main classes of cyclins? |
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Definition
| G1, S-phase, and Mitotic cyclins |
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Term
| Activity of the CDK is regulated by |
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Definition
1. Cyclin Binding
2. Phosphorylation (2 key ones) |
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Term
| What greatly increases the affinity for protein substrates? |
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Definition
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Term
| What is important in control of M-CDK activity, and is caused by the addition of phosphates(2) in the roof of the active site (inhibits activity)? |
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Definition
| Inhibitory Phosphorylation |
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Term
| What removes inhibitory phosphates like Wee1? |
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Definition
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Term
| CDK activity can be suppressed by? |
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Definition
| The binding of CDK inhibitor proteins(CKIs) |
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Term
| CKIs are primarily used in controlling ___ and ____ CDKs |
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Definition
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Term
| When a CKI binds to a CDK what does it do? |
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Definition
| Rearranges structure of the CDK active site and holds the CDK inactive until needed |
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Term
| What are the two distinct enzyme complexes crucial for cell cycle control? And they are both what? |
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Definition
1. APC/C (Anaphase-promoting complex)
2. SCF (S-phase Controlling Factor)
Ubiquitin Ligases |
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Term
| Enzyme complexes can tag proteins with ____. Which targets the protein for destruction in the ____. |
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Definition
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Term
| What is responsible for ubiquitylation and destruction of G1/S-cyclins and certain CKI proteins that control S-phase initiation? |
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Definition
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Term
| What is important in M-phase. Responsible for ubiquitiylation and proteolysis of M-cyclins and other regulators of mitosis? |
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Definition
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Term
| Entry into the M-phase requires this crucial event. |
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Definition
| The activation of Cdc25 which removes the inhibitory phosphate, and the inactivation of Wee1 (kinase) |
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Term
| Cdc25 is activated by phosphorylation via ___ protien kinase. |
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Definition
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Term
| Wee 1 is ____ by phosphorylation. |
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Definition
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Term
| What the family of proteins required for normal chromosome segregation? |
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Definition
| SMC proteins (structural maintenance of chromosomes) |
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Term
| What are the multiprotein complex, overlap with SMC members. ITs phosphorylation is required for condensing activity? |
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Definition
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Term
| What holds sister chromatids together? |
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Definition
|
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Term
| When are cohesions loaded on? |
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Definition
|
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Term
| In the APC/C what does ubiquitin ligase do? |
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Definition
Inactivates protein complexes (cohesins) that connect sister chromatids at metaphase
Also degrades the cohesins to permit the onset of anaphase |
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Term
| Once sister chromatids are separated ____ is activated. |
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Definition
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Term
| Cdh1 is teh specificity factor directs the APC/C to the ___ ___. Cell can begin to ___ mitosis. |
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Definition
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Term
| G1 is a state of stable CDK ___ |
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Definition
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Term
| Where is the function of S-CDK most important? |
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Definition
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Term
| If a cell in S-phase were fused with a cell in G1.... |
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Definition
| the G1 nucleus would immediately enter S-phase, the S-phase nucleus continues DNA replication |
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Term
| If a cell in S-phase were fused with a cell in G2.... |
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Definition
| The G2 nucleus, would stay in G2 , the S-phase nucleus would stay in S-phase |
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Term
| What are the two sensors in the G2 checkpoint? |
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Definition
|
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Term
|
Definition
| By recognizing double strand breaks |
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Term
|
Definition
| By single stranded or unreplicated DNA |
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Term
| ____ are extracellular structures composed of chromatin and granule proteins that bind and kill microorganisms. |
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Definition
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Term
| What is programmed cell death? |
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Definition
|
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Term
| What is cell death following an injury? |
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Definition
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Term
| The presence of phosphatidylserine in the outer leaflet does what? |
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Definition
1. Helps signal nearby cells and macrophages to phagocytose the apoptotic cell. "Eat Me" signal
2. Blocks inflammation, inhibits the production of inflammation-inducing signals (cytokines) by the phagocytic cell |
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Term
| Apotpsis depends on an intracellular proteolytic cascade. Which in turn depends on a family of proteases called? |
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Definition
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Term
| Caspases are synthesized as ____ precursors which are activated by ____ cleavage. |
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Definition
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Term
| What cleave and activate other executioner procaspases, as well as specific target proteins in the cells? |
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Definition
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Term
| What pathway involves extracellular signals that bind to cell-surface receptors? |
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Definition
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Term
| What are the 3 domains of the death receptors? |
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Definition
1. Extracellular ligand-binding domain
2. Single transmembrane domain
3. Intracellular "death" domain |
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Term
| What has a ligand binding domain but not a death domain. It also competitively inhibits the death receptors? |
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Definition
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Term
| What resembles an initiator procaspase, but lacks the proteolytic domain. They also compete with initiator procaspases? |
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Definition
| Intracellular Blocking Proteins (FLIP) |
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Term
| What is activated in response to injury or other stress, and depends on the mitochondria. |
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Definition
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Term
| What family of proteins mediate and regulate mitochondrial outer membrane permeabilization (MOMP) and apoptosis? |
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Definition
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Term
| What two things are essential for MOMP, and directly cause the membrane disruption? |
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Definition
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Term
| What is the only protein that provides the crucial link between apoptotic stimuli and the intrinsic pathway of apoptosis? |
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Definition
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Term
|
Definition
| IAPs (inhibitors of apoptosis proteins0 |
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Term
| As executioner caspases can activate each other (amplification), they must.... |
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Definition
| have mechanisms to limit potential "accidental" activation |
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Term
| Where are IAPs located and what happens when they bind? |
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Definition
| Cytosol, they inhibit any spontaneously activated caspases |
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Term
| The cancer forming process is called? |
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Definition
| Oncogenesis or tumorigenesis |
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Term
| Cancer causing mutations usually occur in what? |
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Definition
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Term
| Certain ____ ____ carried in the germ line increase the probability that cancer will occur at some time. |
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Definition
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Term
| What are the 6 ways tumor cells differ from normal cells? |
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Definition
1. Drive to proliferate
2. Insensitivity to anitgrowth signals
3. Evasion of apoptosis
4. Tissue invasion
5. Angiogenesis
6. Self-sufficiency in growth signals |
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Term
| What tumors derive from epithelia? (lung, breast, stomach) |
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Definition
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|
Term
| What tumors derive from mesenchymal tissues? (bone, cartilage, fat) |
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Definition
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Term
| What tumors that start in the cells of the immune system? |
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Definition
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Term
| Problems with benign tumors arise if their ____ interferes with normal function of if they ____ ____ |
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Definition
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|
Term
| What is the term that describes how tumor cells spread? |
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Definition
|
|
Term
| What is used by cancer cells to penetrate the ECM? |
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Definition
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Term
| Malignant cells usually exhibit the characteristics of? |
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Definition
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Term
| How do tumors arise from stem cells? |
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Definition
| The cells keep dividing and when a mutation occurs they start to accumulate. Then they could turn into cancer cells |
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Term
| As more progenitor cells are made from stem cells what trend do they follow? |
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Definition
| As they increase their degree of differentiation, they start to decline in their replication potential. |
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Term
| What are the 4 ways that cancer can occur as the result of changes in behavior of stem cells? |
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Definition
1. Niche expansion
2. Niche invasion
3. Niche independence
4. Progenitor self renewal |
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Term
| Tumors often arise at sites of ____ or ____ |
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Definition
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|
Term
| Whats expression is induced by low oxygen? |
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Definition
|
|
Term
| What induces transcription of VEGF and is activated by low oxygen? |
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Definition
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Term
| What is the term to describe the time when cells can no longer divide? |
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Definition
|
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Term
| Is APC a proto-oncogene or tumor suppressor? |
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Definition
| Tumor suppressor because you need a loss of function to get the mutant phenotype |
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Term
| When DNA is damaged what prevents the cell from going from G1 to S phase? |
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Definition
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|
Term
| Activation of p53 can lead to ____ |
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Definition
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Term
| What are the 4 ways a proto-oncogene gets converted to a oncogene. |
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Definition
1. Mutation
2. Amplification
3. Chromosomal translocation (fusion making a chimeric protein)
4. Chromosomal translocation (expression by a different promoter that causes misexpression) |
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Term
| What is a dominant oncogene where the glycine at position 12 changed to another amino acid? |
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Definition
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Term
| Ras reduces its GTPas activity and keeps in in the ___ GTP bound state. |
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Definition
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Term
| What promotes cell survival or proliferation, has dominant mutations, arise from point mutations, and cause a gain of function that allows for unregulated cell proliferation and survival? |
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Definition
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Term
| What normally inhibits cell survival and proliferation, mutations are recessive, arises from deletions and point mutations, and causes a loss of function that allows unregulated cell proliferation and survival? |
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Definition
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Term
| What normally repairs are prevents DNA damage, mutations are recessive, arises by deletion and point mutations, and causes a loss of function that allows mutations to accumulate? |
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Definition
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Term
| What when mutated allows for the degradation of beta-catenin and thus leads to the activation of proto-oncogenes? |
|
Definition
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Term
|
Definition
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Term
|
Definition
|
|
Term
| How does ras cause lead to and increase in cancer? |
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Definition
| It reduces the GTPase activity and keeps it in the active GTP bound state. |
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Term
| What adds OH groups to molecules that turns normally harmless molecules to cause damage to DNA? |
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Definition
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|
Term
| What forms when amino acids and creatine react at high temperatures? |
|
Definition
| Heterocyclic amines (HCAs) which are carcinogens |
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|
Term
| What disease causes a disruption in nucleotide repair, which means DNA repair stops functioning properly? |
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Definition
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