IFN-alpha 10 Regulates Immune and Inflammation (G3446)

Target Name: IFNA10

NCBI ID: G3446

IFNA10

IFN-alpha 10 Regulates Immune and Inflammation

The interleukin-8 (IL-8) signaling pathway is a critical factor in the regulation of immune and inflammatory responses. The IL-8 pathway is activated in response to various stimuli, including pathogens, tissue injury, and cancer. One of the key downstream targets of the IL-8 pathway is the cytokine IFN-alpha 10 (IFN-alpha 10), which plays a crucial role in the regulation of immune responses and inflammation.

IFN-alpha 10 is a cytokine that is expressed in various tissues and cells in the body, including immune cells, epithelial cells, and neural cells. It is a key mediator of the IL-8 pathway, participating in the regulation of immune responses, inflammation, and tissue repair.

IFN-alpha 10 functions as a negative regulator of the IL-8 pathway, inhibiting the activity of the downstream signaling kinases, including IRAK4 and IRAK1. These kinases are responsible for the downstream activation of the IL-8 pathway, leading to the production of pro-inflammatory cytokines, such as IL-8, IL-9, and IL-10.

IFN-alpha 10 is able to inhibit the activity of IRAK4 and IRAK1 by a mechanism that is similar to that of the downstream inhibitor p160, which is a well-known inhibitor of the PI3K/Akt signaling pathway. p160 is able to inhibit the activity of IRAK4 and IRAK1 by a mechanism that is similar to that of a competitive inhibitor, binding to the N-terminus of the IRAK4 and IRAK1 proteins and preventing them from interacting with the upstream kinases.

IFN-alpha 10 is able to inhibit the activity of IRAK4 and IRAK1 because it has a unique structure that is able to interact with the upstream kinases in a different manner than does p160. This interaction allows IFN-alpha 10 to inhibit the activity of IRAK4 and IRAK1 while still allowing it to function as a negative regulator of the IL-8 pathway.

IFN-alpha 10 has been shown to play a crucial role in the regulation of immune responses and inflammation. Studies have shown that IFN-alpha 10 is involved in the regulation of a wide range of physiological processes, including immune cell function, inflammation, and tissue repair.

IFN-alpha 10 is involved in the regulation of immune cell function

IFN-alpha 10 is involved in the regulation of the activation and proliferation of immune cells. Studies have shown that IFN-alpha 10 plays a crucial role in the regulation of T cell function, including the regulation of CD4+ and CD8+ T cell proliferation, and the regulation of their survival.

IFN-alpha 10 is able to inhibit the activity of the transcription factor NF-kappa-B, which is involved in the regulation of T cell function. This interaction between IFN-alpha 10 and NF-kappa-B allows for the regulation of T cell proliferation and survival, and is able to prevent excessive T cell proliferation and apoptosis.

IFN-alpha 10 is involved in the regulation of inflammation

IFN-alpha 10 is involved in the regulation of inflammation and is able to prevent the production of pro-inflammatory cytokines. Studies have shown that IFN-alpha 10 is able to inhibit the production of IL-8, IL-9, and IL-10 by the immune cells, including T cells and macrophages.

IFN-alpha 10 is able to inhibit the production of IL-8 by

Protein Name: Interferon Alpha 10

Functions: Produced by macrophages, IFN-alpha have antiviral activities. Interferon stimulates the production of two enzymes: a protein kinase and an oligoadenylate synthetase

The "IFNA10 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 IFNA10 comprehensively, including but not limited to:
•   general information;
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•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
•   disease relevance;
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•   pharmacochemistry experiments;
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•   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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