Are the following statements true or false? 1. A change in intercellular NADPH i

Question

Are the following statements true or false?

1. A change in intercellular NADPH induces a change in the shape of calmodulin.

2. Dimerization of receptor tyrosine kinases activates their threonine phosphatase activity.

3. Since cell types may contain different effectors with similar SH2 domains, the same receptor tyrosine kinase can trigger very different responses in different target cells.

4. G-protein-activated phospholipase C generates diacylglycerol (DAG) which can activate Protein Kinase C.

5. Cyclic AMP is formed by a phosphodiesterase.

6. Activated 7TM-GPCRs cannot bring about changes in gene transcription.

7. Ras is a G protein which is found to be mutated in about half of human cancers; this pro-carcinogenic mutation prevents it from binding GTP.

8. Ryanodine receptors respond to an increase in cytosolic IP3 by releasing ATP from the SER.

9. Irreparable genetic damage, in normal but not some cancer cells, trigger apoptosis via an extrinsic pathway.

Explanation / Answer

Are the following statements true or false?

1. A change in intercellular NADPH induces a change in the shape of calmodulin.---------- false

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2. Dimerization of receptor tyrosine kinases activates their threonine phosphatase activity.---------- true

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3. Since cell types may contain different effectors with similar SH2 domains, the same receptor tyrosine kinase can trigger very different responses in different target cells.------- .---------- true

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4. G-protein-activated phospholipase C generates diacylglycerol (DAG) which can activate Protein Kinase C.

.------- .---------- true

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5. Cyclic AMP is formed by a phosphodiesterase. .---------- false

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6. Activated 7TM-GPCRs cannot bring about changes in gene transcription.

.---------- false

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7. Ras is a G protein which is found to be mutated in about half of human cancers; this pro-carcinogenic mutation prevents it from binding GTP.

.------- .---------- true

=====================================

8. Ryanodine receptors respond to an increase in cytosolic IP3 by releasing ATP from the SER. .---------- true

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9. Irreparable genetic damage, in normal but not some cancer cells, trigger apoptosis via an extrinsic pathway.

.---------- true

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Calmodulin (CaM) : It is a multifunctional intermediate calcium-restricting delegate protein communicated in all eukaryotic cells. It is an intracellular focus of the optional dispatcher Ca2+, and the official of Ca2+ is required for the initiation of Calmodulin. When bound to Ca2+, Calmodulin goes about as a feature of a calcium flag transduction pathway by adjusting its cooperations with different target proteins, for example, kinases or phosphatases

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G protein–coupled receptors (GPCRs) which are otherwise called seven-transmembrane space receptors, 7TM receptors, heptahelical receptors, serpentine receptor, and G protein–linked receptors (GPLR), constitute an extensive protein group of receptors, that sense particles outside the phone and actuate inside flag transduction pathways and, eventually, cell reactions. Coupling with G proteins, they are called seven-transmembrane receptors since they go through the phone layer seven circumstances

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Apoptosis :it is a procedure of modified cell demise that happens in multicellular living beings. Biochemical occasions prompt to trademark cell changes (morphology) and passing. These progressions incorporate blebbing, cell shrinkage, atomic fracture, chromatin buildup, chromosomal DNA discontinuity, and worldwide mRNA rot. Somewhere around 50 and 70 billion cells pass on every day because of apoptosis in the normal human adult.[a] For a normal kid between the ages of 8 and 14, roughly 20 billion to 30 billion cells bite the dust a day.

Two hypotheses of the immediate start of apoptotic systems in well evolved creatures have been recommended: the TNF-actuated (tumor rot figure) show and the Fas-Fas ligand-intervened display, both including receptors of the TNF receptor (TNFR) family[31] coupled to outward flags.

TNF way

TNF-alpha is a cytokine created basically by initiated macrophages, and is the major outward arbiter of apoptosis. Most cells in the human body have two receptors for TNF-alpha: TNFR1 and TNFR2. The official of TNF-alpha to TNFR1 has been appeared to start the pathway that prompts to caspase enactment through the moderate layer proteins TNF receptor-related passing space (TRADD) and Fas-related demise area protein (FADD). cIAP1/2 can restrain TNF- motioning by authoritative to TRAF2. FLIP hinders the initiation of caspase-8. Official of this receptor can likewise in a roundabout way prompt to the enactment of interpretation elements required in cell survival and incendiary responses.However, motioning through TNFR1 may likewise actuate apoptosis in a caspase-free manner.The interface between TNF-alpha and apoptosis indicates why an irregular generation of TNF-alpha assumes a basic part in a few human ailments, particularly in immune system maladies.

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Ras is a group of related proteins which is communicated in all creature cell genealogies and organs. All Ras protein relatives have a place with a class of protein called little GTPase, and are included in transmitting signals inside cells (cell flag transduction). Ras is the prototypical individual from the Ras superfamily of proteins, which are altogether related in 3D structure and manage various cell practices.

At the point when Ras is 'exchanged on' by approaching signs, it in this way switches on different proteins, which at last turn on qualities required in cell development, separation and survival. Changes in ras qualities can prompt to the creation of for all time initiated Ras proteins. Accordingly, this can bring about unintended and overactive motioning inside the phone, even without approaching signs.

Since these signs result in cell development and division, overactive Ras flagging can at last prompt to tumor. The 3 Ras qualities in people (HRas, KRas, and NRas). they are the most widely recognized oncogenes in human malignancy; transformations that forever initiate Ras are found in 20% to 25% of every single human tumor and up to 90% in specific sorts of growth (e.g., pancreatic cancer).For this reason, Ras inhibitors are being examined as a treatment for tumor and different sicknesses with Ras overexpression

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