In the ovary, the FSH receptor is necessary for follicular development and expressed on the granulosa cells.

In the male, the FSH receptor has been identified on the Sertoli cells that are critical for spermatogenesis.

FSH receptors are selectively expressed on the luminal surface of the blood vessels of a wide range of tumors.

Estrogen upregulates FSH receptor sites.

There may be a potential role for suppression of FSH or FSH receptors.

This results in a competition between the follicles and only the follicle with the most FSH receptors survives and is ovulated.

Also, in some women FSH may bind to the FSH receptor site, but be inactive.

The gene is similar to the gene for the FSH receptor and the TSH receptor.

The FSH receptor can also activate the extracellular signal-regulated kinases (ERK).

Elevated FSH receptor levels have been detected in the endothelia of tumor vasculature in a very wide range of solid tumors.

The gene for the LHCGR is found on chromosome 2 p21 in humans, close to the FSH receptor gene.

Polymorphism may affect FSH receptor populations and lead to poorer responses in infertile women receiving FSH medication for IVF.

This hormone stimulates the production of FSH receptors on the follicular granulosa cells and has at the same time a negative feedback on FSH secretion.

Ethinyl estradiol lowers high FSH levels which then, it is theorized, up regulates FSH receptor sites and restores sensitivity to FSH.

No activating mutations of the GnRH receptor in humans have been described in the medical literature, and only one of the FSH receptor has been described, which presented as asymptomatic.

FSH enhances the production of androgen-binding protein by the Sertoli cells of the testes by binding to FSH receptors on their basolateral membranes, and is critical for the initiation of spermatogenesis.

In related studies BMP-6 and BMP-15 were found to block FSH action through inhibiting FSH-dependent adenylate cyclase activity and FSH receptor expression, respectively [ 11 12 ] .

Eventually the FSH level becomes so high that downregulation of FSH receptors occurs and by menopause any remaining small secondary follicles no longer have FSH receptors.)

It is thought that FSH receptors are important in tumor angiogenesis by signalling via two pathways, one involving VEGF, and a Gq/11 mechanism that activates VEGFR-2 independently of VEGF.

The mutant FSH is modified such that it no longer induces Inhibin B production, but the membrane-bound FSH receptors on Sertoli cells still bind to it, delivering the Adjudin directly to the target cells.

Although PGC-2 lack FSH receptors, these cells can serve as a useful in vitro model for GC function, because they produce cAMP in response to forskolin and synthesize progesterone and estradiol when supplied with appropriate substrates.

It is possible, therefore, that the strong expression of FS by the DF may serve to modulate BMP-15 action such that sufficient FSH receptors are expressed in the GC to permit the development of a preovulatory follicle.