describe the role of mitochondria in initiating apoptosis. please describe and summarize in short two paragraphs only.
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describe the role of mitochondria in initiating apoptosis. please describe and summarize in short two paragraphs only.
![The Mitochondria
Play an Initiating
Role in Apoptosis
DNA
damage
Cytochrome c
Apaf-1 (apoptosis
protease activating
factor-1)
Procaspase-9
monomers
(inactive)
Stress
Procaspase-3
Procaspase-7
MK
ATP
Apoptosome causes dimer-
ization of procaspase-9,
creating active caspase-9
dimers.
ROS Developmental
signal
Permeability transition
pore complex opens.
Cytochromec
moves to cytosol.
Binding of cytochrome c
and ATP induces Apaf-1 to
form an apoptosome.
Apoptosome
Caspase-9
dimers
(active)
Caspase-9 catalyzes
proteolytic activation
of caspase-3 and
caspase-7.
These caspases lead to death
and reabsorption of the cell.
Caspase-3
Caspase-7
Cell death](/v2/_next/image?url=https%3A%2F%2Fcontent.bartleby.com%2Fqna-images%2Fquestion%2Fbcdff95c-f0d0-4e03-9572-c23605a53daa%2F1daf58ab-1063-4e67-a141-78c2d0e8b66a%2Faygy3e9_processed.png&w=3840&q=75)
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- Development of the nematode Caenorhabditis ele-gans generates exactly 959 somatic cells; it also producesan additional 131 cells that are later eliminated by apop-tosis. Classical genetic experiments in C. elegans isolatedmutants that led to the identification of the first genesinvolved in apoptosis. Of the many mutations affectingapoptosis in the nematode, none have ever been found inthe gene for cytochrome c. Why do you suppose that sucha central effector molecule in apoptosis was not found inthe many genetic screens for “death” genes that have beencarried out in C. elegans?Stimulation of map kinase can help regulate cell division and cell mass. the following effects of map kinase activation explains an increase in cell mass. Phosphorylation of RSK (kinase and the subsequent phosphorylation of S6 ribosomal subunit. Phosphorylation of myosin light chain Phosphorylation of glyceraldehyde dehydrogenase phosphorylation of histone H1 none of theseDNA damage can suppress the activity of the following cyclin-dependent kinases EXCEPT G1/S-Cdk S-Cdk M-Cdk G1-Cdk Which phenomenon allows the formation of double and triple bonds between carbon atoms? * Reduction Radioactivity Oxidation Hybridization If an agent that disrupts microtubules activity was added to cells at M phase, the cells will ble expected to get arrested at Anaphase O Metaphase O Prophase Telophase O 0 O
- In the normal cycle of Ras activity, when Ras is bound to y activity that removes a phosphate to convert GTP back to GDP and this it is inactive. Activation of Ras involves exchanging GDP for The Ras protein has intrinsic Ras. inactivates activates ATP GTP «< Questic A Moving to another question will save this response. ADP GDP GTPase Clo nucleaseArtificially induced apoptosis (controlled cellular death) is found to be an effective treat- ment for some forms of cancer. Which of the following describes the most likely mechanism by which apoptosis might be induced? A B с D by causing ribosomes to increase the rate of protein synthesis by triggering the division of mitochondria in the cell to increase ATP production by increasing the expression of membrane-bound glucose protein channels by causing lysosomes to release digestive enzymes into the cytosolYou treat human umbilical vein endothelial cells (HUVECS) in the lab with hydrogen peroxide to induce oxidative stress and observe the following: (D) Ctrl H202 4 8. 12 24 Time (h) Which one of the following pathways of cell death are induced in these cells? O Pyroptosis O Apoptosis O Autophagy O Necrosis Caspase-3 activity (relative to control)
- Progression through the cell cycledepends on the phosphorylationof hundreds of different proteins bycyclin–Cdk complexes. What are themolecular mechanisms ensuring thatthese proteins are phosphorylated atprecisely the right time and place?Need help Intaractions of FAK kinase which directly depend on the tyrosine residue 397 (Y397) are inhibbited by a chemical compound in cancercells. Intaraction of FAK kinase with what proteins are blocked by this inhibition? (please give a listt of them all, and that's it)Predict the location(s) (intracellular or extracelular) and a brief description of WHY based on your knowledge of the transport processes in the following constructs. Assume a start codon is present and include any proteolytic processing that would be likely. 1. A PTS1 C-term peroxisomal targeting seq added to C term of a normally secreted protein with usual N -terminal signal sequence 2. Adding of N-terminal mitochondrial targeting sequence to protein with internal nuclear localization seq. 3. Adding N-terminal signal sequence of secreted protein to N-terminus a mitochondria matrix protein precursor with mitochondrial targeting sequence still present
- Multifunctional protein kinases O phosphorylate various targets with the correct consensus sequence carry out phosphorylation as well as sulfonation reactions O remove phosphates through hydrolysis O have a very specific target that they phosphorylate conserve energy in the form of ATP from the degradation of proteinsThe reason why the central effector molecule cytochrome c în apoptosis was not found in the many genetic screens for "death" genes that have been carried out in C. elegansEffects of BPA on phosphorylation of JAK family in RAW264.7 cells
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