Regulation of Tyrosination and Cell Signaling By PTPRJ (G5795)

Target Name: PTPRJ

NCBI ID: G5795

PTPRJ

Regulation of Tyrosination and Cell Signaling By PTPRJ

The protein encoded by the genePTPRJ (Protein Tyrosine Phosphatase and Receptor tyrosine kinase, SCC1) is a key regulator of protein tyrosination, a post-translational modification that plays a crucial role in cell signaling and division. ThePTPRJ gene is located on chromosome 19q31 and has has been implicated in various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders.

PTPRJ is a protein that belongs to thePTP/PIP family, which includes proteins that regulate tyrosination by either dephosphorylating or activating tyrosine phosphatases. These proteins are involved in the of cell signaling pathways, including cell division, apoptosis, and inflammation regulation. ThePTPRJ gene is primarily located in the nucleus and has been shown to be involved in the regulation of cell proliferation, differentiation, and survival.

PTPRJ functions as a negative regulator of the tyrosine kinase Ago1, which is a key enzyme involved in the regulation of cell signaling pathways. Tyrosination is the process by which cells respond to signals from the environment and it is involved in various cellular processes, including cell growth, differentiation, and survival. The tyrosination of various proteins is critical for the regulation of cell signaling pathways and is a key factor in the development and progression of various diseases.

Research has shown that PTPRJ is involved in the regulation of tyrosination and that its dysfunction is associated with the development of various diseases. For example, studies have shown that patients with neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, have reduced levels of PTPRJ . Additionally, studies have shown that patients with certain types of cancer, such as lung and colorectal cancer, have increased levels of PTPRJ.

Furthermore, research has also shown that PTPRJ is involved in the regulation of cell apoptosis. Studies have shown that the levels of PTPRJ are regulated by various factors, including cell stress, DNA damage, and chemoreceptors. Additionally, studies have shown that the dysfunction of PTPRJ is associated with the development of apoptosis.

In addition to its role in cell signaling pathways, PTPRJ is also involved in the regulation of cell division. Studies have shown that the levels of PTPRJ are regulated by the factors, including the cell cycle and the G1/S checkpoint. Additionally, studies have shown that the dysfunction of PTPRJ is associated with the regulation of cell division.

In conclusion, PTPRJ is a protein that is involved in the regulation of various cellular processes, including cell signaling pathways, apoptosis, and cell division. Its dysfunction is associated with the development of various diseases, including cancer and neurodegenerative diseases. Further research is needed to understand the exact role of PTPRJ in these diseases and to develop new therapeutic strategies.

Protein Name: Protein Tyrosine Phosphatase Receptor Type J

Functions: Tyrosine phosphatase which dephosphorylates or contributes to the dephosphorylation of CTNND1, FLT3, PDGFRB, MET, KDR, LYN, SRC, MAPK1, MAPK3, EGFR, TJP1, OCLN, PIK3R1 and PIK3R2 (PubMed:10821867, PubMed:12062403, PubMed:12370829, PubMed:12475979, PubMed:18348712, PubMed:19494114, PubMed:19922411, PubMed:21262971). Plays a role in cell adhesion, migration, proliferation and differentiation (PubMed:12370829, PubMed:14709717, PubMed:16682945, PubMed:19836242). Involved in vascular development (By similarity). Regulator of macrophage adhesion and spreading (By similarity). Positively affects cell-matrix adhesion (By similarity). Positive regulator of platelet activation and thrombosis. Negative regulator of cell proliferation (PubMed:16682945). Negative regulator of PDGF-stimulated cell migration; through dephosphorylation of PDGFR (PubMed:21091576). Positive regulator of endothelial cell survival, as well as of VEGF-induced SRC and AKT activation; through KDR dephosphorylation (PubMed:18936167). Negative regulator of EGFR signaling pathway; through EGFR dephosphorylation (PubMed:19836242). Enhances the barrier function of epithelial junctions during reassembly (PubMed:19332538). Negatively regulates T-cell receptor (TCR) signaling (PubMed:9531590, PubMed:9780142, PubMed:11259588). Upon T-cell TCR activation, it is up-regulated and excluded from the immunological synapses, while upon T-cell-antigen presenting cells (APC) disengagement, it is no longer excluded and can dephosphorylate PLCG1 and LAT to down-regulate prolongation of signaling (PubMed:11259588, PubMed:12913111)

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