Curated Information
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Home > Curated Information Page > PubMed Id: 28052936
Sasaki E, et al. (2017) KLHL3 Knockout Mice Reveal the Physiological Role of KLHL3 and the Pathophysiology of Pseudohypoaldosteronism Type II Caused by Mutant KLHL3. Mol Cell Biol 37 28052936
This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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S71-p - NCCT (mouse)
Modsite: AYEHYANsALPGEPR SwissProt Entrez-Gene
Orthologous residues
NCCT (human): S73‑p, NCCT iso2 (human): S73‑p, NCCT iso3 (human): S73‑p, NCCT (mouse): S71‑p, NCCT (rat): S71‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  kidney
Cellular systems studied:  tissue
Species studied:  mouse
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
KLHL3 (mouse) decrease KLHL3 -/- increase