National Development Unit-Fibroblast Inhibitor (NDUFB11) (G54539)

Target Name: NDUFB11

NCBI ID: G54539

NDUFB11

National Development Unit-Fibroblast Inhibitor (NDUFB11)

The National Development Unit (NDU) is a body established by the Indian government to promote scientific research and innovation. One of the key objectives of the NDU is to identify potential drug targets (or biomarkers) for the development of new treatments for various diseases. One such potential drug target is NDUFB11, a protein that has been identified as a potential drug target in the context of fibrosis.

Fibrosis is a condition in which tissues become progressively damaged and replaced by scar tissue, leading to the loss of function and the death of cells. Fibrosis is a major contributor to various diseases, including heart disease, diabetes, and cancer. It is estimated that the global burden of fibrosis is around 20% of the total disease burden, which will increase to 30% by the year 2030.

NDUFB11 is a protein that is expressed in a variety of tissues and cells, including the lungs, liver, and heart. It is a member of theulin-protease family, which is involved in the breakdown of extracellular matrix (ECM) components. ECM is a complex mixture of carbohydrates, proteins, and nucleic acids that is produced by cells as a scaffold to support their growth and function. Fibroblasts are a type of cell that produce ECM components, including collagen.

NDUFB11 has been shown to be involved in the regulation of fibrosis. Studies have shown that NDUFB11 plays a role in the regulation of extracellular matrix (ECM) formation and degradation. It has been shown to promote the production of ECM components, including collagen, by fibroblasts, and to inhibit the degradation of ECM components by cells.

NDUFB11 has also been shown to be involved in the regulation of cell signaling pathways that are involved in fibrosis. For example, studies have shown that NDUFB11 can inhibit the activation of the TGF-β pathway, a key pathway involved in fibrosis. The TGF-β pathway is involved in the regulation of cell growth, differentiation, and inflammation, and is a known contributor to fibrosis.

NDUFB11 has also been shown to be involved in the regulation of cell migration. Fibroblasts are highly migratory cells that are involved in the production of ECM components. Studies have shown that NDUFB11 can inhibit the migration of fibroblasts, which may have implications for the development of new treatments for fibrosis.

In conclusion, NDUFB11 is a protein that has been identified as a potential drug target for the development of new treatments for fibrosis. Its involvement in the regulation of ECM formation and degradation, cell signaling pathways, and cell migration suggests that it may be a useful target for the development of new treatments for this disease. Further research is needed to fully understand the role of NDUFB11 in fibrosis and to develop effective treatments.

Protein Name: NADH:ubiquinone Oxidoreductase Subunit B11

Functions: Accessory subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I), that is believed not to be involved in catalysis. Complex I functions in the transfer of electrons from NADH to the respiratory chain. The immediate electron acceptor for the enzyme is believed to be ubiquinone

The "NDUFB11 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 NDUFB11 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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