TLS Online TPP Program

#Question id: 1518


Following statements are regarding to the some cancers harbor characteristic chromosome alterations. Chronic myelogenous leukemia (CML), a common leukemia in humans, was found to be associated with the Philadelphia chromosome.

A. Philadelphia chromosome is generated by a translocation between chromosomes 22 and 9. The two chromosomes exchange their terminal regions, which leads to a characteristic alteration in the size of chromosome 9.

B. At the breakpoint of this translocation, a new fusion protein, the BCR-ABL fusion, is generated.

C. The BCR-ABL fusion protein is a constitutively active kinase that phosphorylates multiple signal-transducing proteins.

D. If this translocation occurs in a hematopoietic cell in the bone marrow, the activity of the chimeric BCR-ABL oncogene dephosphorylate proteins thereby activating many intracellular signal-transducing proteins.

Which of the following statements are incorrect?

#Unit 4. Cell Communication and Cell Signaling
  1. A and B

  2. A and D

  3. A and C

  4. D only

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TLS Online TPP Program

#Question id: 2858

#Unit 2. Cellular Organization

When lactose enters the cell, it is converted to allolactose. It is allolactose (rather than lactose itself) that controls the Lac repressor. Paradoxically, the conversion of lactose to allolactose is catalyzed by b-galactosidase, itself encoded by one of the lac genes. How is this possible? Which statement is incorrect according lac genes expressions?

TLS Online TPP Program

#Question id: 2859

#Unit 2. Cellular Organization

NtrC controls expression of genes involved in nitrogen metabolism by inducing a conformational change in a pre-bound RNA polymerase, triggering transition to the open complex.

I. Under low nitrogen level condition, NtrC is phosphorylated by a kinase, NtrB,

II. NtrC (bound to its sites upstream) interacts directly with s54. This requires that the DNA between the activator binding sites and the promoter form a loop to accommodate the interaction

III. Active NtrC binds four sites located approximately 150 bp upstream of the glnA gene.

IV. NtrC itself has an ATPase activity which provides the energy needed to induce a conformational change in polymerase.

Correct series of Activation by NtrC is;

TLS Online TPP Program

#Question id: 2860

#Unit 2. Cellular Organization

 Lactose metabolism in E. coli is carried out by two enzymes, with possible involvement by a third. The genes for all three enzymes are clustered together and transcribed together from one promoter, yielding a polycistronic message. These three genes, linked in function, are therefore also linked in expression. They are turned off and on together.

Negative control

keeps the lac operon repressed in the absence of lactose.

positive control

keeps the operon relatively inactive in the presence of glucose, even when lactose is present.

when all the glucose is gone and lactose is present, a mechanism should exist.

is mediated by a factor called catabolite activator protein (CAP), which, in conjunction with cyclic-AMP, stimulates transcription.

TLS Online TPP Program

#Question id: 2861

#Unit 2. Cellular Organization

What is the result of regulatory mutation in given lac operon in merodiploids

TLS Online TPP Program

#Question id: 2862

#Unit 2. Cellular Organization

What is the result of regulatory mutation in given lac operon in merodiploids,

TLS Online TPP Program

#Question id: 2863

#Unit 2. Cellular Organization

The promoter of the araBAD operon from E. coli is activated in the presence of arabinose and the absence of glucose and directs expression of genes encoding enzymes required for arabinose metabolism. Unlike the cases of lac and gal genes, where a repressor and an activator work together, here two activators work together: AraC and CAP

+ arabinose

AraC binds that sugar and adopts a configuration that allows it to bind DNA as a dimer to the adjacent half-sites, araI1 and araI2

– arabinose

the AraC dimer adopts a different conformation and binds to araO2 and araI1, there is no monomer at site araI2, and so the protein cannot activate the araBAD promoter (araPBAD). This promoter is also controlled by CAP.