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Mol Bio Ch 17-18
Molecular Biology Chapters 17-18
| Question | Answer |
|---|---|
| Cell surface breaks up into membrane enclosed fragments called | apoptotic bodies |
| Cells swell and burst spilling their content | Necrosis (accidental cell death) |
| Apoptotic cells are biochemically | 1. Detection of cleaved DNA by gel-electrophoresis. 2=TUNEL assay (TdT-mediated dUTP Nick End Labeling). 3=Detection of Annexin V. |
| During apoptosis endonucleases cleaves | chromosomal DNA in linker regions between nucleosomes |
| The enzyme ___ ___ ___ adds chains of labeled dUTP to the 3’-OH ends of DNA fragment. | terminal deoxynucleotidyl transferase (TdT) |
| binds phosphatidylserine and can be labeled for detection. | Annexin V |
| Apoptosis is activated through two major signaling pathways | Intrinsic and Extrinsic |
| Intrinsic pathway is triggered from | within the cell by stress or DNA damage |
| Extrinsic pathway is activated when | a pro-apoptotic ligand binds to a pro-apoptotic receptor |
| Caspases are intracellular enzymes that trigger | cell death |
| Caspases are proteases that have a ___ at their active site and cleave their target proteins at specific ___ ___. | cysteine; aspartic acids |
| Procaspases which operate in start of proteolytic cascades are called | Initiator Capases |
| When activated, initiator caspases cleave and activate ___ ___ which cleaves target proteins. | executioner caspases |
| Cell-surface death receptors activate the | extrinsic pathway of apoptosis |
| Extracellular signals bind to ____ ____on cell surface and trigger ___ ___. | death receptors; extrinsic pathway |
| Death receptors are transmembrane proteins that contain ___ ___ which are required receptor to activate apoptosis. These receptors belong to ___ ( ___ ___ ___) family of receptors. | death domain; TNF (Tumor Necrosis Factor) |
| Intrinsic pathway of Apoptosis depends on | Mitochondria |
| When cytochrome-c released into cytosol, it binds to procaspase activating adaptor protein called ____. This binding causes Apaf1 to oligomerize to form wheel like heptamer called ___. | Apaf1; apoptosome |
| Intrinsic pathway is stimulated by the release of | cytochrome C from mitochondria |
| Apaf1 in apoptosome recruits ___ ___ ___ which in turn activates downstream ___ ___ to induce apoptosis | initiator procaspase 9; executioner procaspases |
| Intrinsic pathway of apoptosis is regulated by ___ family of proteins | Bcl2 |
| Two properties of cancer cells | They reproduce in defiance of normal constraints on cell growth and They invade and colonize territories normally reserved for other cells. |
| A ___ glandular tumor remains inside the basal lamina that marks the boundary of the normal structure. | benign |
| A ___ glandular tumor destroys duct integrity and spreads to other tissues. | malignant |
| secondary tumors derived from cells that break off of the primary tumor – make cancer hard to eradicate. | Metastases |
| derive from epithelial cells (e.g. breast, digestive organs). | Carcinomas |
| derive from connective tissue or muscle cells. | Sarocomas |
| derive from white blood cells. | Leukemias and lymphomas |
| Cancer typically requires | more than one mutation in a given cell to trigger uncontrolled growth |
| An example of an ____ change is the formation of heterochromatin, which leads to highly compact DNA that is poorly expressed. | epigenetic |
| ___ ___ ___ are capable of indefinite self-renewal, but they also produce a large number of transit amplifying cells with limited capacity for self-renewal. As a consequence, most cells in a tumor are not capable of independently forming tumors. | Cancer stem cells |
| Tumors induce ____ or the development of new blood vessels that feed the tumor. As the tumor grows, it becomes hypoxic and this initiates a signaling pathway that directs the formation of new blood vessels. | angiogenesis |
| Proto-oncogenes: overactive or overexpressed forms of these genes promote cancer and are called | oncogenes |
| inactive forms of these genes contribute to cancer development. | Tumor Suppressor Genes |
| Characterization of hereditary retinoblastoma led to the discovery of | Tumor Suppressor Genes |
| Phosphoinositide 3-kinase (PI 3-kinase)/ Akt intracellular signaling pathway is critical | Controlling cell growth |
| One of the main signaling pathways activated by growth factors is __ __, which activates ___ pathway. ___ activates other genes that stimulate protein synthesis and inhibit protein degradation. | PI3 kinases; TOR; TOR |
| Akt drives cell growth by | 1Stimulating glucose uptake 2Increased glucose utilization 3Conversion of excess citric acid into acetyl CoA |
| ___ ___ dephosphorylates the molecules that PI3 kinase phosphorylates. In total, it limits Akt activation and hence controls cell proliferation. | PTEN phosphatase |
| The p53 protein is a transcription factor that regulates the transcription of many genes including ___. | p21 |
| The p21 gene encodes a protein p21, that | inhibits G1/S and S-Cdk. This stalls the cell cycle and even leads to cell death unless the DNA damage is repaired. |
| p53 induces apoptosis | by inactivating anti-apoptotic Bcl2 protein |
| Replication of damaged DNA leads to? | Chromosomal abnormalities such as activation of oncogenes or loss of tumor suppressor genes. |