Target Name: SCHIP1
NCBI ID: G29970
Review Report on SCHIP1 Target / Biomarker Content of Review Report on SCHIP1 Target / Biomarker
SCHIP1
Other Name(s): FLJ39160 | Schwannomin interacting protein 1, transcript variant 4 | SCHIP1 variant 1 | Schwannomin interacting protein 1, transcript variant 3 | Schwannomin-interacting protein 1 (isoform 1) | SCHIP-1 | Schwannomin interacting protein 1, transcript variant 1 | SCHIP1 variant 3 | SCHIP1 variant 4 | Schwannomin-interacting protein 1 | SCHI1_HUMAN | schwannomin interacting protein 1

SCHIP1: A Potential Drug Target for Various Diseases

SCHIP1 (Spermidine-Residue-Containing Input Region 1) is a protein that is expressed in various cell types of the human body, including neurons, endothelial cells, and epithelial cells. It is a key regulator of the cell cycle, and it is involved in the progression of cancer.

Recent studies have identified SCHIP1 as a potential drug target for various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. Its unique mechanism of action, as well as its widespread expression across different cell types, make it an attractive target for drug development.

One of the key reasons for the interest in SCHIP1 is its involvement in the regulation of the cell cycle. The cell cycle is the process by which cells grow, divide, and replicate their genetic material. During the cell cycle, cells go through several stages , including G1, S, G2, and M. At each stage, Schip1 plays a critical role in regulating the progress of the cell.

SCHIP1 is a key regulator of the G1 stage of the cell cycle. It is involved in the regulation of the cyclin D1-CDK4 complex, which is responsible for activating the G1 phase. Additionally, it is involved in the regulation of the cyclin D2- CDK6 complex, which is responsible for activating the S phase.

SCHIP1 is also involved in the regulation of the G2 stage of the cell cycle. It is involved in the regulation of the cyclin B2-CDK1 complex, which is responsible for activating the G2 phase.

SCHIP1 is a key regulator of the M stage of the cell cycle. It is involved in the regulation of the cyclin A-CDK4 complex, which is responsible for metaphase entry and the start of the cytoplasmic phase.

In addition to its role in regulating the cell cycle, SCHIP1 is also involved in the regulation of cell survival. Studies have shown that SCHIP1 is involved in the regulation of cell survival by promoting the formation of mitochondrial-associated protein (MAP) complex.

SCHIP1 is also involved in the regulation of angiogenesis, which is the process by which new blood vessels are formed. Studies have shown that SCHIP1 is involved in the regulation of angiogenesis by promoting the formation of blood vessels in the skin and in the regulation of blood vessel permeability.

In conclusion, SCHIP1 is a protein that is involved in the regulation of the cell cycle, cell survival, and angiogenesis. Its unique mechanism of action and its widespread expression across different cell types make it an attractive target for drug development. Further studies are needed to fully understand the role of SCHIP1 in the regulation of the cell cycle and the regulation of various diseases.

Protein Name: Schwannomin Interacting Protein 1

The "SCHIP1 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 SCHIP1 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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