F11 receptor

From WikiMD's Wellness Encyclopedia

F11 Receptor is a protein that in humans is encoded by the F11R gene. It is also known as Junctional Adhesion Molecule A (JAM-A) and is a member of the immunoglobulin superfamily.

Function[edit | edit source]

The F11 receptor is a type of protein that plays a crucial role in the tight junctions between cells in the body. These tight junctions are important for maintaining the integrity of tissues and organs, and they also play a role in the immune response. The F11 receptor is involved in the process of cell adhesion, which is the process by which cells interact and attach to neighbouring cells through specialized molecules on their surfaces.

Structure[edit | edit source]

The F11 receptor is a type of transmembrane protein, which means it spans the entire width of the cell membrane. It has two extracellular immunoglobulin domains, a single transmembrane domain, and a short cytoplasmic tail. The extracellular domains are involved in the adhesion process, while the cytoplasmic tail is thought to be involved in intracellular signaling.

Clinical significance[edit | edit source]

Alterations in the F11 receptor have been associated with a variety of diseases, including cancer, inflammatory bowel disease, and atherosclerosis. In cancer, for example, overexpression of the F11 receptor has been observed in several types of tumors, suggesting it may play a role in tumor progression. In inflammatory bowel disease, alterations in the F11 receptor may disrupt the integrity of the intestinal barrier, leading to inflammation.

Research[edit | edit source]

Research into the F11 receptor is ongoing, with scientists seeking to better understand its role in health and disease. This research could potentially lead to the development of new treatments for diseases associated with alterations in the F11 receptor.


References[edit | edit source]


External links[edit | edit source]

  • F11R at the National Center for Biotechnology Information
  • F11R at UniProt

See also[edit | edit source]

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