What does the p16 gene do?

What does the p16 gene do?

p16 is a tumor suppressor protein that plays an important role in regulating the cell circle. As a CDK inhibitor, p16 can slow down the progression of the cell cycle by inactivating the CDK that phosphorylates the retinoblastoma protein, which is also a tumor suppressor protein that regulates the cell circle.

Is p16 a tumor-suppressor gene?

The p16 (CDKN2a/INK4a) gene is an important tumor-suppressor gene, involved in the p16/cyclin-dependent kinase/retinoblastoma gene pathway of cell cycle control. The p16 protein is considered to be a negative regulator of the pathway.

Do humans have p16?

3-D STRUCTURE OF HUMAN TUMOR-SUPPRESSOR PROTEIN PRODUCED The gene is the p16 tumor-suppressor gene. The protein produced by this gene, the p16 protein, normally prevents cells from dividing when they shouldn’t.

What is p53 and p16?

p53/p21/p16 tumor suppressors in control of the G1/S cell–cycle checkpoint. The tumor-suppressor proteins p53, p21, and p16 are major regulators of the G1/S cell–cycle checkpoint.

Why is p16 overexpressed in HPV?

Among over 100 different HPV types, HPV-16 and HPV-18 are detected in the majority of HPV-positive SCCHNs. The p16 gene is often mutated in SCCHN, its overexpression is caused by the viral E7 protein. Consequently, p16 is assumed to be an indirect marker of HPV-induced SCCHN.

What is INK4A?

The most well-studied are the p16(INK4A) and the p14(ARF) proteins. Both function as tumor suppressors, which means they keep cells from growing and dividing too rapidly or in an uncontrolled way. Both proteins are also involved in stopping cell division in older cells (senescence).

What is p16 in HPV?

Expression of p16INK4A (p16 positive) is highly correlated with human papilloma virus (HPV) infection in head and neck squamous cell carcinoma (HNSCC), however, p16-positivity is not limited to HPV positive tumors and therefore, not a perfect surrogate for HPV.

What type of protein is p16 INK4A?

The tumor suppressor protein p16INK4a (inhibitor of CDK4) is one of the most direct links between cell-cycle control and cancer. The p16INK4a gene is frequently inactivated in human tumors, and inheritance of mutant alleles results in susceptibility to several types of cancer.

How is p16 regulated?

p16 protein is relatively stable and its expression is primary regulated by transcriptional control. Polycomb group (PcG) proteins associate with the p16 locus in a long non-coding RNA, ANRIL-dependent manner, leading to repression of p16 transcription.

What is p53 p21 pathway?

The p53/p21 Pathway Plays an Important Role in Cell Senescence of BM-MSCs from SLE Patients. It is reported that the p53/p21 pathway plays an important role in regulated BM-MSCs senescence process.

Is p16 the same as HPV?

What does the p16INK4a gene do?

The p16INK4a gene is frequently inactivated in human tumors, and inheritance of mutant alleles results in susceptibility to several types of cancer. p16INK4a is part of a cell-cycle regulatory pathway that converges in the tumor suppressor protein Rb. The mechanisms that regulate p16INK4a are starting to be characterized. Publication types

Is p16 INK4a a tumor suppressor protein?

Currently, p16 Ink4a is considered a tumor suppressor protein because of its physiological role and downregulated expression in a large number of tumors. Intriguingly, overexpression of p16 Ink4a has also been described in several tumors.

How does p16 INK4a inhibit the S phase?

It is well known that p16 Ink4a contributes to the regulation of cell cycle progression by inhibiting the S phase. The molecular pathway responsible for this inhibition is shown in Figure 1. Briefly, p16 Ink4a binds to CDK4/6, inhibiting cyclin D–CDK4/6 complex formation and CDK4/6-mediated phosphorylation of Rb family members.

What is the molecular mechanism of p16 INK4a overexpression in HPV-related neoplasms?

(ii) The molecular mechanism that explains p16 Ink4a overexpression in HPV-related neoplasms is the presence of viral oncoproteins E6 and E7. Rb protein is inactivated by interaction with the high-risk HPV oncoprotein E7, and oncoprotein E6 induces degradation of the tumor suppressor p53.

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