ARHGAP22-IT1: A Drug Target / Disease Biomarker (G100689073)

Target Name: ARHGAP22-IT1

NCBI ID: G100689073

ARHGAP22-IT1

Other Name(s): ARHGAP22 intronic transcript 1

ARHGAP22-IT1: A Drug Target / Disease Biomarker

ARHGAP22-IT1 is a protein that is expressed in various tissues of the body, including the brain, heart, and kidneys. It is a member of the ARHGAP22 family of proteins, which are known for their role in intracellular signaling.

One of the key functions of ARHGAP22-IT1 is its role in the regulation of cell signaling pathways. This protein has been shown to play a role in the regulation of several different signaling pathways, including the TGF-β pathway and the PI3K/Akt pathway.

The TGF-β pathway is a well-known signaling pathway that is involved in the regulation of cell growth, differentiation, and survival. This pathway is activated by the binding of the protein TGF-β to its receptor, which is a protein called ECT in the case of mammals.

ARHGAP22-IT1 has been shown to play a role in the regulation of TGF-β signaling by interacting with the protein Smad2. This interaction between ARHGAP22-IT1 and Smad2 allows for the regulation of TGF-β signaling by ARHGAP22-IT1.

The PI3K/Akt pathway is a signaling pathway that is involved in the regulation of cell survival and proliferation. This pathway is activated by the binding of the protein PI3K to its receptor, which is a protein called AKT in the case of mammals.

ARHGAP22-IT1 has also been shown to play a role in the regulation of PI3K/Akt signaling by interacting with the protein p120. This interaction between ARHGAP22-IT1 and p120 allows for the regulation of PI3K/Akt signaling by ARHGAP22-IT1.

In addition to its role in the regulation of TGF-β and PI3K/Akt signaling pathways, ARHGAP22-IT1 has also been shown to play a role in the regulation of several other signaling pathways, including the FERMT3 pathway and the S1/S6 signaling pathway.

The FERMT3 pathway is a signaling pathway that is involved in the regulation of cell division and the maintenance of cellular order. This pathway is activated by the binding of the protein FERMT3 to its receptor, which is a protein called Fyn in the case of mammals.

ARHGAP22-IT1 has been shown to play a role in the regulation of FERMT3 signaling by interacting with the protein Mar10. This interaction between ARHGAP22-IT1 and Mar10 allows for the regulation of FERMT3 signaling by ARHGAP22-IT1.

The S1/S6 signaling pathway is a signaling pathway that is involved in the regulation of cell signaling pathways. This pathway is activated by the binding of the protein S1 to its receptor, which is a protein called S100 in the case of mammals.

ARHGAP22-IT1 has also been shown to play a role in the regulation of S1/S6 signaling pathway by interacting with the protein Calbindin. This interaction between ARHGAP22-IT1 and Calbindin allows for the regulation of S1/S6 signaling pathway by ARHGAP22-IT1.

In conclusion, ARHGAP22-IT1 is a protein that has been shown to play a role in the regulation of several different signaling pathways, including TGF-β, PI3K/Akt, FERMT3, and S1/S6. These signaling pathways are involved in the regulation of cell growth, differentiation, and survival, and ARHGAP22-IT1 is

Protein Name: ARHGAP22 Intronic Transcript 1

The "ARHGAP22-IT1 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 ARHGAP22-IT1 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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