Full 2L QBank
Pathology General a2ae6145

True about p53 -a) Tumor suppressor geneb) Protooncogenec) Proapoptoticd) Encodes 53KDe) Arrest cell cycle in G1

A
bce
B
bde
C
abcd
D
acde
High-Yield Explanation
p 53 is a tumor suppressor gene and it is aproapoptotic factor, i.e. it promotes apoptosis if repair of DNA damage is unsuccessful at G1 arrest.   The name p53 is in reference to its apparent molecular mass; it runs as a 53 kilodalton (Kda) protein on SDS-page. But based on calculations from its amino acid residues, p53's mass is actually only 43.7 K Da.   P53 (Guardian of the Genome /Molecular Policeman)   The p53 gene is located on the short arm (p) of chromosome 17(17pl3.1)   It is the most common target for genetic alteration in human tumors Q A little over 50% of human tumors contain mutations in this gene The p53   gene derives its name from its apparent molecular mass (It is a 53 k D protein) Q The major functional activities of the p53 protein are cell -cycle arrest & initiation of apoptosis in response to DNA damage Normal (Wild Type)   it function as a tumor suppressor gene & function as a critical gatekeeper against the deveiopment of cancel Q The p53 gene is located in the nucleus & functions   as a nuclear transcription factor Two major functions are: In blocking mitotic activity: p53 inhibit cyclins & cyclin dependent kinase(CDK)   & prevents the cell to enter G1 phase transiently'' .This allow the normal cell to repair the DNA damage In promoting apoptosis :   p53 gene directs cells that have damaged DNA to apoptosis by activating apoptosis inducing BAX genes & thus brings the defective cells to an end.   This process operates in the cell cycle at G1 & G2 phase before the cell enters theS or M phase Q Mutant p53 gene    The wild type of p53 gene may undergo mutations that inactivates or alter the normal function of p53   Presence of mutant p53 gene in tumor celts predicts apoor response to radiotherapy & chemotherapy (poor prognostic factor) Q   Inheritance of one mutant p53 allele predisposes individua Is to develop malignant tumors because only one additional hit is needed to inactivate   the second normal allele- second hit phenomenon Q Most p53 mutation are acquired in somatic cells that inactivate or alter the normal function of p53   gene Tumors expressing mutantp53 genes are more resistant to radiation therapy & chemotherapy than tumors with wild type p53

Related Pathology MCQs

Practice 2,00,000+ NEET PG Questions Free

Timed mock tests, mistake queue analytics, audio lectures & zero attempt limits on i❤️Exams.

Start Free Mock Test Now