hSET2: A Potential Drug Target for Various Diseases (G29072)

Target Name: SETD2

NCBI ID: G29072

SETD2

hSET2: A Potential Drug Target for Various Diseases

Setd2 (hSET2) is a gene that has been identified as a potential drug target or biomarker for various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. The gene is located on chromosome 12 and encodes a protein known as heat shock factor 2 (HSF2).

HSF2 is a protein that plays a crucial role in the regulation of cellular stress responses. It helps to prevent cells from undergoing programmed cell death, which is a natural response to stress and damage. During times of stress, HSF2 helps to promote the expression of genes that help cells to repair and regenerate themselves.

Research has shown that hSET2 is involved in a wide range of physiological processes in the body, including cell growth, differentiation, and survival. It has been shown to play a role in the development and progression of various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases.

One of the key reasons for the interest in hSET2 as a potential drug target is its involvement in the regulation of cellular stress responses. Many diseases, including cancer, are caused by the failure of cells to respond to stress and damage in a timely manner. This can lead to the development of harmful mutations, which can lead to the growth and progression of cancer cells.

In addition to its role in the regulation of cellular stress responses, hSET2 has also been shown to play a role in the development and progression of neurodegenerative disorders. Studies have shown that hSET2 is involved in the regulation of the neurotransmitter system, which is responsible for transmitting signals between cells in the brain. This suggests that hSET2 may be involved in the development and progression of neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease.

Another potential drug target for hSET2 is its role in the regulation of cellular immune responses. Studies have shown that hSET2 is involved in the regulation of T cell development and function. This suggests that hSET2 may be involved in the development and regulation of autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis.

In conclusion, hSET2 is a gene that has been identified as a potential drug target or biomarker for a wide range of diseases. Its involvement in the regulation of cellular stress responses, neurodegenerative disorders, and immune responses makes it an attractive target for drug development. Further research is needed to fully understand the role of hSET2 in these diseases and to develop safe and effective treatments.

Protein Name: SET Domain Containing 2, Histone Lysine Methyltransferase

Functions: Histone methyltransferase that specifically trimethylates 'Lys-36' of histone H3 (H3K36me3) using dimethylated 'Lys-36' (H3K36me2) as substrate (PubMed:16118227, PubMed:19141475, PubMed:21526191, PubMed:21792193, PubMed:23043551, PubMed:27474439). It is capable of trimethylating unmethylated H3K36 (H3K36me0) in vitro (PubMed:19332550). Represents the main enzyme generating H3K36me3, a specific tag for epigenetic transcriptional activation (By similarity). Plays a role in chromatin structure modulation during elongation by coordinating recruitment of the FACT complex and by interacting with hyperphosphorylated POLR2A (PubMed:23325844). Acts as a key regulator of DNA mismatch repair in G1 and early S phase by generating H3K36me3, a mark required to recruit MSH6 subunit of the MutS alpha complex: early recruitment of the MutS alpha complex to chromatin to be replicated allows a quick identification of mismatch DNA to initiate the mismatch repair reaction (PubMed:23622243). Required for DNA double-strand break repair in response to DNA damage: acts by mediating formation of H3K36me3, promoting recruitment of RAD51 and DNA repair via homologous recombination (HR) (PubMed:24843002). Acts as a tumor suppressor (PubMed:24509477). H3K36me3 also plays an essential role in the maintenance of a heterochromatic state, by recruiting DNA methyltransferase DNMT3A (PubMed:27317772). H3K36me3 is also enhanced in intron-containing genes, suggesting that SETD2 recruitment is enhanced by splicing and that splicing is coupled to recruitment of elongating RNA polymerase (PubMed:21792193). Required during angiogenesis (By similarity). Required for endoderm development by promoting embryonic stem cell differentiation toward endoderm: acts by mediating formation of H3K36me3 in distal promoter regions of FGFR3, leading to regulate transcription initiation of FGFR3 (By similarity). In addition to histones, also mediates methylation of other proteins, such as tubulins and STAT1 (PubMed:27518565, PubMed:28753426). Trimethylates 'Lys-40' of alpha-tubulins such as TUBA1B (alpha-TubK40me3); alpha-TubK40me3 is required for normal mitosis and cytokinesis and may be a specific tag in cytoskeletal remodeling (PubMed:27518565). Involved in interferon-alpha-induced antiviral defense by mediating both monomethylation of STAT1 at 'Lys-525' and catalyzing H3K36me3 on promoters of some interferon-stimulated genes (ISGs) to activate gene transcription (PubMed:28753426)

The "SETD2 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 SETD2 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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