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Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. Additionally we are shipping Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 Antibodies (88) and many more products for this protein.
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Data suggest underlying pathology for some patients with type II Bartter syndrome is linked to stability of ROMK1 in ERAD pathway; using a yeast expression system, cells can be rescued by wild-type (rat) ROMK1 but not by ROMK1 containing any one of four mutations found in (human) type II Bartter syndrome; mutant ROMKs are significantly less stable than wild-type ROMK. (ERAD = endoplasmic reticulum-associated degradation)
WNK4 (show WNK4 Proteins) is a substrate of SFKs and the association of c-Src (show SRC Proteins) and PTP-1D (show PTPN11 Proteins) with WNK4 (show WNK4 Proteins) at Tyr (show TYR Proteins)(1092) and Tyr (show TYR Proteins)(1143) plays an important role in modulating the inhibitory effect of WNK4 (show WNK4 Proteins) on ROMK
knockdown of KCNJ1 in HK-2 (show HK2 Proteins) cells promoted cell proliferation. Collectively, these data highlight that KCNJ1, low-expressed in ccRCC and associated with poor prognosis, plays an important role in ccRCC cell growth and metastasis
The association between polymorphisms in KCNJ1, SLC12A1 (show SLC12A1 Proteins), and 7 other genes and calcium intake and colorectal neoplasia risk was studied.
A KCNJ1 SNP was associated with increased FG during HCTZ treatment.
Molecular analysis revealed a compound heterozygous mutation in the KCNJ1 gene, consisting of a novel K76E and an already described V315G mutation, both affecting functional domains of the channel protein.
Findings suggest that 11q24 is a susceptible locus for openness, with KCNJ1 as the possible candidate gene.
no mutation in the KCNJ1 gene, among patients suffering from bartter and Gitelman syndromes
PI3K (show PIK3CA Proteins)-activating hormones inhibit ROMK by enhancing its endocytosis via a mechanism that involves phosphorylation of WNK1 (show WNK1 Proteins) by Akt1 (show AKT1 Proteins) and SGK1 (show SGK1 Proteins).
THGP (show UMOD Proteins) modulation of ROMK function confers a new role of THGP (show UMOD Proteins) on renal ion transport and may contribute to salt wasting observed in FJHN/MCKD-2 (show UMOD Proteins)/GCKD patients.
The findings support ROMK as the pore-forming subunit of the cytoprotective mitoK(ATP) channel in heart mitochondria.
The results provide evidence that NHERF1 (show SLC9A3R2 Proteins) mediates K(+) current activity through acceleration of the surface expression of ROMK1 K(+) channels in M-1 cells.
ENaC (show SCNN1A Proteins) and ROMK channel activity in kidney tubules are inhibited in TgWnk4(pseudoaldosteronism type II) mice. Wnk4 (show WNK4 Proteins)(PHAII)-induced inhibition of ENaC (show SCNN1A Proteins) and ROMK may contribute to the suppression of K(+) secretion in the tubules.
The differential regulation of ROMK, large-conductance Ca(2 (show CA2 Proteins)+)-activated K(+) (BK) channel (show KCNMA1 Proteins), BK-alpha and NKCC2 (show SLC12A1 Proteins) between female and male mice, at least, were partly mediated via WNK1 (show WNK1 Proteins) pathway, which may contribute to the sexual dimorphism of plasma K(+) and blood pressure control.
Suggest that the hyperkalemia in knock-in mouse with the CUL3 (show CUL3 Proteins)(Delta403-459) mutation is not caused by reduced ROMK expression in the distal nephron.
animal knockouts of ROMK1 do not produce Bartter phenotype. ROMK1 is critical in response to high K intake-stimulated K+ secretion in the collecting tubule.
Lovastatin stimulates ROMK1 channels by inducing PI(4,5)P2 synthesis, suggesting that the drug could reduce cyclosporine-induced nephropathy.
ROMK1 protein abundance and activity are down-regulated by SPAK (show STK39 Proteins) and OSR1 (show OSR1 Proteins)
It was concluded that miR-194 regulates ROMK channel activity by modulating ITSN1 expression thereby enhancing ITSN1/WNK-dependent endocytosis.
hypertension resistance sequence variants inhibit ROMK channel function by different mechanisms
Kcnj1 is expressed in cells associated with osmoregulation and acts as a K+ efflux pathway that is important in maintaining extracellular levels of potassium ion in the developing embryo.
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. It is activated by internal ATP and probably plays an important role in potassium homeostasis. The encoded protein has a greater tendency to allow potassium to flow into a cell rather than out of a cell. Mutations in this gene have been associated with antenatal Bartter syndrome, which is characterized by salt wasting, hypokalemic alkalosis, hypercalciuria, and low blood pressure. Multiple transcript variants encoding different isoforms have been found for this gene.
ATP-regulated potassium channel ROM-K
, ATP-sensitive inward rectifier potassium channel 1
, inward rectifier K(+) channel Kir1.1
, inwardly rectifying K+ channel
, potassium channel, inwardly rectifying subfamily J member 1
, potassium inwardly-rectifying channel, subfamily J, member 1
, potassium inwardly-rectifying channel J1
, ATP-sensitive inward rectifier potassium channel 1-like
, K+ channel protein
, Potassium inwardly-rectifying channel subfamily J
, inwardly rectifying potassium channel ROMK-2
, potassium inwardly-rectifying channel, subfamily J, member 15
, LOW QUALITY PROTEIN: ATP-sensitive inward rectifier potassium channel 1