Prolactin receptor

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Prolactin Receptor (PRLR) is a type of protein that in humans is encoded by the PRLR gene. It is a member of the cytokine receptor family. The prolactin receptor is associated with several key biological processes, including lactation and immune system regulation.

Structure[edit | edit source]

The Prolactin Receptor is a single-pass transmembrane receptor that is structurally similar to other members of the cytokine receptor family. It consists of an extracellular domain, a transmembrane domain, and an intracellular domain. The extracellular domain is responsible for binding to prolactin, while the intracellular domain is involved in signal transduction.

Function[edit | edit source]

The primary function of the Prolactin Receptor is to bind to prolactin, a hormone produced by the pituitary gland. This binding triggers a series of intracellular events, leading to the activation of various signaling pathways, including the JAK-STAT signaling pathway, the MAPK/ERK pathway, and the PI3K/AKT/mTOR pathway. These pathways are involved in a variety of biological processes, such as cell growth, differentiation, and survival.

In addition to its role in lactation, the Prolactin Receptor is also involved in the regulation of the immune system. It has been found to be expressed in various immune cells, including T cells, B cells, and natural killer cells, and its activation has been shown to modulate immune responses.

Clinical significance[edit | edit source]

Mutations in the PRLR gene have been associated with several diseases, including breast cancer, prostate cancer, and infertility. In particular, overexpression of the Prolactin Receptor has been observed in various types of cancer, suggesting a potential role in tumorigenesis.

Furthermore, the Prolactin Receptor has been identified as a potential therapeutic target for various diseases. For example, drugs that inhibit the activity of the Prolactin Receptor are currently being investigated for the treatment of breast cancer.

See also[edit | edit source]

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