In web search, finding a large number of documents with very little relevant information is termed:

TLS Online TPP Program

#Question id: 15441

#Unit 4. Cell Communication and Cell Signaling

In hermaphrodites, expression of the egl-1 gene in the neurons is repressed by the transcription factor, and deletion of that causes these neurons to undergo apoptosis;

TLS Online TPP Program

#Question id: 15369

#Unit 4. Cell Communication and Cell Signaling

Changes in DNA methylation, as well as changes in the activity of histone-modifying enzymes or chromatin-remodeling complexes, are major drivers of tumorigenesis,

a. Hypermethylation of CpG dinucleotides of TSG gene causes cancer.

b. Hypomethylation of CpG dinucleotides of proto-oncogenes causes cancer.

c. SWI/SNF plays a role in repressing the expression of E2F genes.

d. Gain of SWI/SNF function, just like loss of Rb function.

Which of the statements are INCORRECT;

TLS Online TPP Program

#Question id: 15368

#Unit 4. Cell Communication and Cell Signaling

Recent evidence from humans and mice has strongly implicated the SNF5 gene in cancer. The SNF5 protein is a core member of the;

TLS Online TPP Program

#Question id: 15367

#Unit 4. Cell Communication and Cell Signaling

Genes whose protein products stimulate apoptosis behave as tumor suppressors, An example is the PTEN gene, The phosphatase encoded by this gene dephosphorylates phosphatidylinositol 3,4,5-trisphosphate, a secondary messenger that functions in activation of AKT, cells lacking PTEN phosphatase shows; EXCEPT

TLS Online TPP Program

#Question id: 15366

#Unit 4. Cell Communication and Cell Signaling

For pro-proliferation signaling pathways to cause uncontrolled proliferation, as is seen in cancer, this p53 up-regulation must not occur, It is therefore not surprising that p53 is inactive in most human tumors through loss of p53 function itself, down-regulation of positive regulators (PR) of p53 or up-regulation of negative regulators (NR) of p53, these regulators are accordingly

TLS Online TPP Program

#Question id: 15365

#Unit 4. Cell Communication and Cell Signaling

The MDM2 protein in its active form can form a complex with p53, inhibiting the transcription factor and causing p53 ubiquitinylation and subsequent proteasomal degradation, ATM phosphorylates MDM2 to inactivate it, causing increased stabilization of p53, but there is one another gene or key regulator which controls the level of MDM2;