#Question id: 1522
#Unit 4. Cell Communication and Cell Signaling
Conversion of a proto-oncogene into an oncogene, also called activation, generally involves a gain-of-function mutation. Following statements are regarding to the mechanisms that produce oncogenes from the corresponding proto-oncogenes.
A. A change in a single base pair in a proto-oncogene that results in a hyperactive or constitutively active protein product.
B. A chromosomal translocation that fuses two genes together to produce a hybrid gene encoding a chimeric protein whose activity, unlike that of the parent proteins, is permanently suppress.
C. A chromosomal translocation that brings a growth regulatory gene under the control of alternative enhancers that cause inappropriate expression of the gene.
D. Amplification of a DNA segment including a proto-oncogene so that numerous copies exist, leading to overproduction of the encoded protein.
Which of the following statements are correct?
#Question id: 1523
#Unit 4. Cell Communication and Cell Signaling
Following statements are regarding to the apoptosis which is induced by trophic factors.
A. The presence of specific trophic factors (e.g., NGF) leads to activation of their cognate receptor tyrosine kinases (e.g., TrkA) and activation of the PKB pathway.
B. DNA damage or ultraviolet irradiation leads to induction of synthesis of the BH3-only Puma protein. Puma binds to Bak and Bax as well as to Bcl-2, allowing Bak and Bax to form oligomeric pores.
C. Removal of a cell from its substratum disrupts integrin signaling, leading to release of the BH3-only Bim protein from the cytoskeleton.
D. Binding of extracellular death signals, such as tumor necrosis factor and Fas ligand, to their receptors oligomerizes an associated protein (FADD), which in turn triggers the caspase cascade, leading to cell murder by apoptosis.
Which of the following pathway does not belong to the trophic factor inducing apoptotic pathway?
#Question id: 1524
#Unit 4. Cell Communication and Cell Signaling
Tumor-suppressor genes generally encode proteins that in one way or another inhibit cell proliferation. Loss-of-function mutations in one or more of these proliferation inhibitory proteins contribute to the development of many cancers. Prominent among the classes of proteins encoded by tumor-suppressor genes are:
A. Intracellular proteins that regulate or inhibit entry into the cell cycle
B. Receptors or signal transducers for secreted hormones or developmental signals that inhibit cell proliferation
C. Checkpoint pathway proteins that arrest the cell cycle if DNA is damaged
D. Proteins that promote apoptosis
Following genes belongs to the above class-
i. p53
ii. Rb
iii.TGF- β
iv. Caspase 3 and 7
which of the following match is correct?
#Question id: 1525
#Unit 4. Cell Communication and Cell Signaling
Following statements are regarding to chromatin remodelling factors SWI/SNF complexes. Which one of them is incorrect?
#Question id: 1526
#Unit 4. Cell Communication and Cell Signaling
Following statements are regarding to apoptosis.
A. In the worm apoptotic pathway, CED-3 (caspase-9 in mammals) is a protease required to destroy cell components during apoptosis.
B. CED-4 (Apaf-1) was able to accelerate the autoproteolytic cleavage and activation of purified CED-9
C. Once EGL-1 causes dissociation of the CED-4/CED-9 complex, the released CED-4 dimer joins with three other CED-4 dimers to make an octamer, which then activates CED-3
D. Many apoptotic stimuli lead to damage of the outer mitochondrial membrane, causing release into the cytosol of several proteins that stimulate apoptosis. In particular, cytochrome c released from mitochondria activates Apaf-1, which in turn activates caspase-3 and 7.
Which of the following combination is incorrect?
#Question id: 1527
#Unit 4. Cell Communication and Cell Signaling
Following are the six fundamental properties of malignant tumors. Which of these properties are amenable to study in a cell culture model of cancer?
(I) self-sufficiency in growth signals
(II) insensitivity to antigrowth signals
(III) evasion of apoptosis
(IV) limitless replicative potential
(V) sustained angiogenesis
(VI) tissue invasion and metastasis