Animal Studies On Epo Receptor Mutations
Mice with truncated EpoR are viable, which suggests Jak2 activity is sufficient to support basal erythropoiesis by activating the necessary pathways without phosphotyrosine docking sites being needed. EpoR-H form of EpoR truncation contains the first, and, what can be argued, the most important tyrosine 343 that serves as a docking site for the Stat5 molecule, but lacks the rest of the cytoplasmic tail. These mice exhibit elevated erythropoiesis consistent with the idea that phosphatase recruitment (and therefore the shutting down of signaling) is aberrant in these mice.
The EpoR-HM receptor also lacks the majority of the cytoplasmic domain, and contains the tyrosine 343 that was mutated to phenylalanine, making it unsuitable for efficient Stat5 docking and activation. These mice are anemic and show poor response to hypoxic stress, such as phenylhydrazine treatment or erythropoietin injection.
Read more about this topic: Erythropoietin Receptor
Famous quotes containing the words animal, studies and/or receptor:
“... found myself
myself, smaller,
not thin but thinner, nervous,
who hurries without animal calm.”
—Denise Levertov (b. 1923)
“...Women’s Studies can amount simply to compensatory history; too often they fail to challenge the intellectual and political structures that must be challenged if women as a group are ever to come into collective, nonexclusionary freedom.”
—Adrienne Rich (b. 1929)
“The disinterest [of my two great-aunts] in anything that had to do with high society was such that their sense of hearing ... put to rest its receptor organs and allowed them to suffer the true beginnings of atrophy.”
—Marcel Proust (1871–1922)