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Publication : Murine Surf4 is essential for early embryonic development.

First Author  Emmer BT Year  2020
Journal  PLoS One Volume  15
Issue  1 Pages  e0227450
PubMed ID  31978056 Mgi Jnum  J:284050
Mgi Id  MGI:6389148 Doi  10.1371/journal.pone.0227450
Citation  Emmer BT, et al. (2020) Murine Surf4 is essential for early embryonic development. PLoS One 15(1):e0227450
abstractText  Newly synthesized proteins co-translationally inserted into the endoplasmic reticulum (ER) lumen may be recruited into anterograde transport vesicles by their association with specific cargo receptors. We recently identified a role for the cargo receptor SURF4 in facilitating the secretion of PCSK9 in cultured cells. To examine the function of SURF4 in vivo, we used CRISPR/Cas9-mediated gene editing to generate mice with germline loss-of-function mutations in Surf4. Heterozygous Surf4+/- mice exhibit grossly normal appearance, behavior, body weight, fecundity, and organ development, with no significant alterations in circulating plasma levels of PCSK9, apolipoprotein B, or total cholesterol, and a detectable accumulation of intrahepatic apoliprotein B. Homozygous Surf4-/- mice exhibit embryonic lethality, with complete loss of all Surf4-/- offspring between embryonic days 3.5 and 9.5. In contrast to the milder murine phenotypes associated with deficiency of known SURF4 cargoes, the embryonic lethality of Surf4-/- mice implies the existence of additional SURF4 cargoes or functions that are essential for murine early embryonic development.
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