The antiserum was produced against synthesized peptide derived from human HNF4 alpha around the phosphorylation site of Ser313. AA range:280-329

Phospho-HNF4-α (S313) Polyclonal Antibody detects endogenous levels of HNF4-α protein only when phosphorylated at S313.The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):LRsQV

HNF4A

Hepatocyte nuclear factor 4-alpha

HNF4A ;
HNF4 ;
NR2A1 ;
TCF14 ;
Hepatocyte nuclear factor 4-alpha ;
HNF-4-alpha ;
Nuclear receptor subfamily 2 group A member 1 ;
Transcription factor 14 ;
TCF-14 ;
Transcription factor HNF-4

The protein encoded by this gene is a nuclear transcription factor which binds DNA as a homodimer. The encoded protein controls the expression of several genes, including hepatocyte nuclear factor 1 alpha, a transcription factor which regulates the expression of several hepatic genes. This gene may play a role in development of the liver, kidney, and intestines. Mutations in this gene have been associated with monogenic autosomal dominant non-insulin-dependent diabetes mellitus type I. Alternative splicing of this gene results in multiple transcript variants encoding several different isoforms. [provided by RefSeq, Apr 2012],

Alternative products:Additional isoforms seem to exist,Disease:Defects in HNF4A are the cause of maturity onset diabetes of the young type 1 (MODY1) [MIM:125850]; also shortened MODY-1. MODY [MIM:606391] is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age) and a primary defect in insulin secretion. The clinical phenotype of MODY1 is characterized by severe insulin secretory defects, and by major hyperglycemia associated with microvascular complications.,Function:Transcriptionally controlled transcription factor. Binds to DNA sites required for the transcription of alpha 1-antitrypsin, apolipoprotein CIII, transthyretin genes and HNF1-alpha. May be essential for development of the liver, kidney and intestine.,miscellaneous:Binds fatty acids.,online information:Hepatocyte nuclear factors entry,PTM:Phosphorylated on tyrosine residue(s); phosphorylation is important for its DNA-binding activity. Phosphorylation may directly or indirectly play a regulatory role in the subnuclear distribution.,similarity:Belongs to the nuclear hormone receptor family.,similarity:Belongs to the nuclear hormone receptor family. NR2 subfamily.,similarity:Contains 1 nuclear receptor DNA-binding domain.,subunit:Homodimerization is required for HNF4-alpha to bind to its recognition site.,

Nucleus.

Kidney,Liver,

>>AMPK signaling pathway ;
>>Maturity onset diabetes of the young