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KLHL3 is ubiquitously expressed and encodes a full-length protein which has an N-terminal BTB domain followed by a BACK domain and six kelch-like repeats in the C-terminus. Additionally we are shipping KLHL3 Proteins (5) and many more products for this protein.
Showing 10 out of 65 products:
Human Polyclonal KLHL3 Primary Antibody for IHC, WB - ABIN2775874
Schmutz, Martin, Terry, Couronne, Grimwood, Lowry, Gordon, Scott, Xie, Huang, Hellsten, Tran-Gyamfi, She, Prabhakar, Aerts, Altherr, Bajorek, Black, Branscomb, Caoile, Challacombe, Chan, Denys et al.: The DNA sequence and comparative analysis of human chromosome 5. ... in Nature 2004
Human Polyclonal KLHL3 Primary Antibody for WB - ABIN2781023
Lai, Orelli, Till, Godley, Fernald, Pamintuan, Le Beau: Molecular characterization of KLHL3, a human homologue of the Drosophila kelch gene. in Genomics 2000
KLHL3 regulates paracellular chloride transport in the kidney by ubiquitination of claudin-8 (show CLDN8 Antibodies)
increased protein expression levels of WNK1 (show WNK1 Antibodies) and WNK4 (show WNK4 Antibodies) kinases cause PHAII by KLHL3 R528H mutation due to impaired KLHL3-Cullin3-mediated ubiquitination.
Data indicate that WNK lysine deficient protein kinase 4 protein (WNK4) was degraded not only by proteasomes but also by atypical protein kinase C scaffold protein p62 (p62)-kelch-like 3 protein (KLHL3)-mediated selective autophagy.
Familial hyperkalemia and hypertension caused by KLHL3 mutations is accompanied by hypercalciuria as well as hyperkalemia and hypertension.
Akt (show AKT1 Antibodies) and PKA phosphorylated KLHL3 at S433, and phosphorylation of KLHL3 by PKA inhibited WNK4 (show WNK4 Antibodies) degradation.
KLHL3 is phosphorylated at serine 433 in the Kelch domain (a site frequently mutated in hypertension with hyperkalemia) by protein kinase C (show PKC Antibodies) in cultured cells and that this phosphorylation prevents WNK4 (show WNK4 Antibodies) binding and degradation.
Hyperkalemic hypertension-associated cul3 (show CUL3 Antibodies) mutations depletes KLHL3, preventing WNK degradation, despite increased CUL3 (show CUL3 Antibodies)-mediated WNK ubiquitylation.
CUL3 (show CUL3 Antibodies) and KLHL3 gene products are physiologically important regulators of thiazide-sensitive distal nephron sodium chloride reabsorption.
analysis of how mutations of KLHL3 show less ability to ubiquitinate WNK4 (show WNK4 Antibodies) because of KLHL3's low stability and/or decreased binding to CUL3 (show CUL3 Antibodies) or WNK4 (show WNK4 Antibodies)
Disease causing mutations in human KLHL3 disrupt the interaction with CUL3 (show CUL3 Antibodies), a crystallographic study.
KLHL3 is a substrate adaptor for WNK4 in a ubiquitin E3 ligase complex
CUL3 (show CUL3 Antibodies) and KLHL3 have roles in in electrolyte homeostasis and in Pseudohypoaldosteronism type II
This gene is ubiquitously expressed and encodes a full-length protein which has an N-terminal BTB domain followed by a BACK domain and six kelch-like repeats in the C-terminus. These kelch-like repeats promote substrate ubiquitination of bound proteins via interaction of the BTB domain with the CUL3 (cullin 3) component of a cullin-RING E3 ubiquitin ligase (CRL) complex. Muatations in this gene cause pseudohypoaldosteronism type IID (PHA2D)\; a rare Mendelian syndrome featuring hypertension, hyperkalaemia and metabolic acidosis. Alternative splicing results in multiple transcript variants encoding distinct isoforms.
kelch-like protein 3
, kelch-like 3