Target Name: TRAJ31
NCBI ID: G28724
Review Report on TRAJ31 Target / Biomarker Content of Review Report on TRAJ31 Target / Biomarker
TRAJ31
Other Name(s): T cell receptor alpha joining 31

Traj31: A Key Regulator of T Cell Function

Traj31, also known as T cell receptor alpha joining 31, is a protein that is expressed in T cells, a type of white blood cell that plays a crucial role in the immune system. T cells are responsible for recognizing and responding to foreign substances in the body, and their activity is crucial for maintaining both physical and mental health. Traj31 is a key regulator of T cell function, and it has been identified as a potential drug target or biomarker for a variety of diseases.

The immune system is a complex process that involves the activation and proliferation of T cells. Once T cells are activated, they undergo a process called clonal expansion, during which they divide and produce new T cells. This process is regulated by the Traj31 protein. Traj31 helps to ensure that T cells divide and proliferate in a controlled and orderly manner, and it has been shown to play a role in the regulation of T cell sensitivity to drugs such as chemotherapy and radiation.

In addition to its role in T cell proliferation, Traj31 is also involved in the regulation of T cell differentiation. T cells are able to differentiate into different types based on the presence or absence of specific signaling molecules. Traj31 helps to ensure that T cells differentiate into the correct type, and it has been shown to play a role in the regulation of T cell differentiation into CD4+ T cells, which are a critical part of the immune system.

Traj31 has also been shown to play a role in the regulation of T cell responses to foreign substances. When T cells encounter a foreign substance, such as a virus or a cancer cell, they are activated and begin to divide and produce new T cells. Traj31 helps to ensure that these T cells respond appropriately to the foreign substance, and it has been shown to play a critical role in the regulation of T cell responses to viruses and cancer cells.

In addition to its role in T cell function, Traj31 has also been shown to play a role in the regulation of T cell survival. T cells are a vital part of the immune system, and they are sensitive to a variety of stresses, such as exposure to radiation or chemotherapy. Traj31 helps to ensure that T cells survive these stresses and continue to function properly, and it has been shown to play a critical role in the regulation of T cell survival.

Traj31 has also been shown to play a role in the regulation of T cell plasticity, which is the ability of T cells to change and adapt in response to new challenges. T cells are able to change their responsibilities and develop new functions based on the presence or absence of specific signaling molecules. Traj31 helps to ensure that T cells are able to change and adapt in response to new challenges, and it has been shown to play a critical role in the regulation of T cell plasticity.

In conclusion, Traj31 is a protein that plays a critical role in the regulation of T cell function. It helps to ensure that T cells divide and proliferate in a controlled and orderly manner, and it has been shown to play a role in the regulation of T cell sensitivity to drugs, T cell differentiation, response to foreign substances, and survival. Traj31 is also involved in the regulation of T cell plasticity, and it has been shown to be a potential drug target or biomarker for a variety of diseases. Further research is needed to fully understand the role of Traj31 in the immune system and its potential as a drug.

Protein Name: T Cell Receptor Alpha Joining 31

Functions: J region of the variable domain of T cell receptor (TR) beta chain that participates in the antigen recognition (PubMed:24600447). Alpha-beta T cell receptors are antigen specific receptors which are essential to the immune response and are present on the cell surface of T lymphocytes. Recognize peptide-major histocompatibility (MH) (pMH) complexes that are displayed by antigen presenting cells (APC), a prerequisite for efficient T cell adaptive immunity against pathogens (PubMed:25493333). Binding of alpha-beta TR to pMH complex initiates TR-CD3 clustering on the cell surface and intracellular activation of LCK that phosphorylates the ITAM motifs of CD3G, CD3D, CD3E and CD247 enabling the recruitment of ZAP70. In turn ZAP70 phosphorylates LAT, which recruits numerous signaling molecules to form the LAT signalosome. The LAT signalosome propagates signal branching to three major signaling pathways, the calcium, the mitogen-activated protein kinase (MAPK) kinase and the nuclear factor NF-kappa-B (NF-kB) pathways, leading to the mobilization of transcription factors that are critical for gene expression and essential for T cell growth and differentiation (PubMed:23524462). The T cell repertoire is generated in the thymus, by V-(D)-J rearrangement. This repertoire is then shaped by intrathymic selection events to generate a peripheral T cell pool of self-MH restricted, non-autoaggressive T cells. Post-thymic interaction of alpha-beta TR with the pMH complexes shapes TR structural and functional avidity (PubMed:15040585)

The "TRAJ31 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 TRAJ31 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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