TNFRSF13B: A Protein Regulating Immune and Inflammatory Response

Target Name: TNFRSF13B

NCBI ID: G23495

TNFRSF13B: A Protein Regulating Immune and Inflammatory Response

TNFRSF13B (Transient Activator of Nuclear Factor Activated T-Cell Signaling 13B), also known as TR13B_HUMAN, is a protein that plays a crucial role in the regulation of cellular immune responses and inflammation. Discovered in 2005, TNFRSF13B is a member of the TNF receptor family, which is involved in the regulation of immune and inflammatory responses.tnfrsf13b (TR13B_HUMAN), is a protein that plays a crucial role in the regulation of cellular immune responses and inflammation. Discovered in 2005, TNFRSF13B is a member of the TNF receptor family, which is involved in the regulation of immune and inflammatory responses.

TNFRSF13B is a 21-kDa transmembrane protein that is expressed in various tissues and cells, including immune cells, neurons, and epithelial cells. The protein is composed of an extracellular domain, a transmembrane domain, and an intracellular domain. The extracellular domain is involved in the formation of the protein's N-terminus, while the transmembrane domain is responsible for the protein's structural stability and functions as a receptor. The intracellular domain is involved in the protein's interaction with other cellular signaling pathways.

TNFRSF13B is involved in the regulation of cellular immune responses and inflammation by modulating the activity of several transcription factors, including NF-kappa-B, AP-1, and NF-IL-6. The protein has been shown to play a role in the regulation of T cell development, activation, and differentiation.

One of the most significant functions of TNFRSF13B is its ability to regulate the activity of NF-kappa-B, a transcription factor that plays a central role in the regulation of inflammation and immune responses. NF-kappa-B is activated by various factors, including TNFRSF13B, and this activation can induce the production of pro-inflammatory cytokines.

TNFRSF13B has also been shown to regulate the activity of AP-1, a transcription factor that is involved in the regulation of cell growth and differentiation. The interaction between TNFRSF13B and AP-1 has been shown to play a role in the regulation of cellular processes such as cell growth, apoptosis, and inflammation.

In addition to its role in regulating NF-kappa-B and AP-1, TNFRSF13B has also been shown to play a role in the regulation of NF-IL-6, a transcription factor that is involved in the regulation of inflammation. The interaction between TNFRSF13B and NF-IL-6 has been shown to play a role in the regulation of cellular inflammation and the development of inflammatory diseases.

TNFRSF13B is also involved in the regulation of the production of pro-inflammatory cytokines, such as TNF-伪 and IL-12. The protein has been shown to play a role in the regulation of the production of these cytokines by promoting the activation and activation of various transcription factors, including NF-kappa-B and AP-1.

TNFRSF13B is also involved in the regulation of cellular apoptosis, which is the process by which cells die as a result of various stimuli, including intrinsic and extrinsic factors. The protein has been shown to play a role in the regulation of apoptosis by modulating the activity of several transcription factors, including NF-kappa-B and AP-1.

TNFRSF13B is also involved in the regulation of cellular signaling pathways that are involved in the regulation of inflammation and immune responses. The protein has been shown to play a role in the regulation of several signaling pathways, including T cell signaling pathways and the regulation of inflammation.

TNFRSF13B is a potential drug target and

Protein Name: TNF Receptor Superfamily Member 13B

Functions: Receptor for TNFSF13/APRIL and TNFSF13B/TALL1/BAFF/BLYS that binds both ligands with similar high affinity. Mediates calcineurin-dependent activation of NF-AT, as well as activation of NF-kappa-B and AP-1. Involved in the stimulation of B- and T-cell function and the regulation of humoral immunity

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