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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 and many more products for this protein.
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However, phosphorylation of SPAK (show STK39 Antibodies) and NCC (show SLC12A3 Antibodies) at distal convoluted tubules were almost completely absent even in WNK4 (show WNK4 Antibodies)(-/-)KLHL3(R528H/R528H) mice. In conclusion, increased WNK1 (show WNK1 Antibodies) was unable to compensate for WNK4 (show WNK4 Antibodies) deficiency and phosphorylate the NCC (show SLC12A3 Antibodies), indicating that WNK4 (show WNK4 Antibodies) is indispensable for the onset of PHAII.
the heterozygous deletion of KLHL3 was not sufficient to cause PHAII, indicating that autosomal dominant type pseudohypoaldosteronism type II (PHAII) is caused by the dominant negative effect of mutant KLHL3.
Potassium depletion stimulates NCC (show SLC12A3 Antibodies) via phosphorylation and inactivation of the KLHL3 and promoting increased blood pressure.
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.
A new recessive mutation in KLHL3 (S553L) was identified in familial hyperkalemia and hypertension. Increased urinary NCC (show SLC12A3 Antibodies) was found in affected members (heterozygous) with dominant KLHL3 Q309R, and in affected members (homozygous) of the recessive form.
Mutation in the KLHL3 gene is associated with Gordon syndrome.
The results demonstrate that Hcy decreases the expression of cMyBP-C through a KLHL3-mediated ubiquitin-proteasome pathway, and thereby influences heart development.
This study provides substantial new insights into the role of phosphorylation of KLHL3 in regulating the interaction with WNK4 (show WNK4 Antibodies)
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 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.
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