Target Name: PMS2
NCBI ID: G5395
Review Report on PMS2 Target / Biomarker Content of Review Report on PMS2 Target / Biomarker
PMS2
Other Name(s): Postmeiotic segregation increased 2 nirs variant 6 | Mismatch repair endonuclease PMS2 (isoform f) | Mismatch repair endonuclease PMS2 (isoform j) | MMRCS4 | PMSL2 | Mismatch repair endonuclease PMS2 (isoform b) | Mismatch repair endonuclease PMS2 | PMS2 variant 10 | PMS-2 | PMS1 homolog 2, mismatch repair system component | Mismatch repair endonuclease PMS2 (isoform c) | PMS2 variant 2 | PMS1 homolog 2, mismatch repair system component, transcript variant 3 | PMS2 variant 8 | Mismatch repair endonuclease PMS2 (isoform a) | PMS2 variant 7 | HNPCC4 | LYNCH4 | PMS2 postmeiotic segregation increased 2 | PMS2 variant 1 | PMS2 variant 12 | PMS2 variant 5 | PMS1 homolog 2, mismatch repair system component, transcript variant 4 | PMS1 homolog 2, mismatch repair system component, transcript variant 6 | PMS1 homolog 2, mismatch repair system component, transcript variant 13 | PMS2CL | Mismatch repair endonuclease PMS2 (isoform i) | Mismatch repair endonuclease PMS2 (isoform e) | Colorectal cancer, hereditary nonpolyposis, type 4 | PMS1 homolog 2, mismatch repair system component, transcript variant 7 | PMS2 variant 13 | PMS1 homolog 2, mismatch repair system component, transcript variant 14 | PMS2 variant 4 | PMS1 homolog 2, mismatch repair system component, transcript variant 9 | Mismatch repair endonuclease PMS2 (isoform h) | PMS1 homolog 2, mismatch repair system component, transcript variant 8 | PMS1 protein homolog 2 | PMS1 homolog 2, mismatch repair system component, transcript variant 1 | PMS2 variant 9 | PMS2 variant 14 | Mismatch repair endonuclease PMS2 (isoform d) | PMS1 homolog 2, mismatch repair system component, transcript variant 11 | postmeiotic segregation increased 2 nirs variant 6 | PMS1 homolog 2, mismatch repair protein | Postmeiotic segregation increased (S. cerevisiae) 2 | DNA mismatch repair protein PMS2 | Mismatch repair endonuclease PMS2 (isoform g) | MLH4 | PMS2 variant 11 | PMS1 homolog 2, mismatch repair system component, transcript variant 10 | PMS2_HUMAN | PMS1 homolog 2, mismatch repair system component, transcript variant 5 | PMS1 homolog 2, mismatch repair system component, transcript variant 2 | PMS1 homolog 2, mismatch repair system component, transcript variant 12 | PMS2 variant 6 | PMS2 variant 3

PMS2: A Drug Target / Disease Biomarker

Premenstrual syndrome (PMS) is a common hormonal disorder that affects many women, characterized by physical symptoms such as bloating, cramps, and mood swings, as well as emotional symptoms such as anxiety and depression. Despite the significant impact that PMS has on women's quality of life, there is currently no cure or effective treatment available.

One potential drug target for PMS is PMS2, which is a protein that is expressed in the placenta and has been shown to play a role in the development and maintenance of PMS. PMS2 has been shown to interact with several other hormones, including estrogen and progesterone, which are also involved in the development of PMS symptoms.

In addition to its potential as a drug target, PMS2 has also been identified as a potential biomarker for PMS. The detection and quantification of PMS2 in the placenta could potentially serve as a diagnostic tool for PMS and could also be used to monitor the effectiveness of potential treatments.

The study of PMS2 and its potential as a drug target or biomarker is still in its early stages, but it holds great promise for the future treatment of PMS. future studies are being conducted to further understand the role of PMS2 in the development and progression of PMS, as well as its potential as a drug target.

In conclusion, PMS2 is a protein that has the potential to be a drug target or biomarker for PMS. Further research is needed to understand its role in the development and progression of PMS and its potential as a treatment.

Protein Name: PMS1 Homolog 2, Mismatch Repair System Component

Functions: Component of the post-replicative DNA mismatch repair system (MMR) (PubMed:30653781, PubMed:35189042). Heterodimerizes with MLH1 to form MutL alpha. DNA repair is initiated by MutS alpha (MSH2-MSH6) or MutS beta (MSH2-MSH3) binding to a dsDNA mismatch, then MutL alpha is recruited to the heteroduplex. Assembly of the MutL-MutS-heteroduplex ternary complex in presence of RFC and PCNA is sufficient to activate endonuclease activity of PMS2. It introduces single-strand breaks near the mismatch and thus generates new entry points for the exonuclease EXO1 to degrade the strand containing the mismatch. DNA methylation would prevent cleavage and therefore assure that only the newly mutated DNA strand is going to be corrected. MutL alpha (MLH1-PMS2) interacts physically with the clamp loader subunits of DNA polymerase III, suggesting that it may play a role to recruit the DNA polymerase III to the site of the MMR. Also implicated in DNA damage signaling, a process which induces cell cycle arrest and can lead to apoptosis in case of major DNA damages. Possesses an ATPase activity, but in the absence of gross structural changes, ATP hydrolysis may not be necessary for proficient mismatch repair (PubMed:35189042)

The "PMS2 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about PMS2 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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