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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 Proteins (10) and many more products for this protein.
Showing 10 out of 85 products:
Dog (Canine) Polyclonal KCNJ1 Primary Antibody for WB - ABIN2776290
Tobin, Tomaszewski, Braund, Hajat, Raleigh, Palmer, Caulfield, Burton, Samani: Common variants in genes underlying monogenic hypertension and hypotension and blood pressure in the general population. in Hypertension 2008
Human Polyclonal KCNJ1 Primary Antibody for ELISA, WB - ABIN451810
Ji, Foo, ORoak, Zhao, Larson, Simon, Newton-Cheh, State, Levy, Lifton: Rare independent mutations in renal salt handling genes contribute to blood pressure variation. in Nature genetics 2008
The findings support ROMK as the pore-forming subunit of the cytoprotective mitoK(ATP) channel in heart mitochondria.
WNK4 (show WNK4 Antibodies) is a substrate of SFKs and the association of c-Src (show SRC Antibodies) and PTP-1D (show PTPN11 Antibodies) with WNK4 (show WNK4 Antibodies) at Tyr (show TYR Antibodies)(1092) and Tyr (show TYR Antibodies)(1143) plays an important role in modulating the inhibitory effect of WNK4 (show WNK4 Antibodies) on ROMK
knockdown of KCNJ1 in HK-2 (show HK2 Antibodies) 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 Antibodies), 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 Antibodies)-activating hormones inhibit ROMK by enhancing its endocytosis via a mechanism that involves phosphorylation of WNK1 (show WNK1 Antibodies) by Akt1 (show AKT1 Antibodies) and SGK1 (show SGK1 Antibodies).
THGP (show UMOD Antibodies) modulation of ROMK function confers a new role of THGP (show UMOD Antibodies) on renal ion transport and may contribute to salt wasting observed in FJHN/MCKD-2 (show UMOD Antibodies)/GCKD patients.
KCNJ1 mutations are associated with Bartter syndrome.
Suggest that the hyperkalemia in knock-in mouse with the CUL3 (show CUL3 Antibodies)(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 Antibodies) and OSR1 (show OSR1 Antibodies)
It was concluded that miR (show MLXIP Antibodies)-194 regulates ROMK channel activity by modulating ITSN1 (show ITSN1 Antibodies) expression thereby enhancing ITSN1 (show ITSN1 Antibodies)/WNK-dependent endocytosis.
hypertension resistance sequence variants inhibit ROMK channel function by different mechanisms
Absence of small conductance K+ channel (show KCNC4 Antibodies) (SK) activity in apical membranes of thick ascending limb and cortical collecting duct in knockout mice a model for bartter's disease__
SGK-1 (show SGK1 Antibodies) phosphorylation of ROMK drives expression on the plasmalemma; because SGK-1 (show SGK1 Antibodies) is an early aldosterone-induced gene, results suggest a possible molecular mechanism for aldosterone-dependent regulation of the secretory potassium channel (show KCNAB2 Antibodies) in the kidney
ROMK is required for functional expression of the 70-pS K channel (show KCNC4 Antibodies) in the thick ascending limb.
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.
potassium inwardly-rectifying channel, subfamily J, member 1
, spliced potassium channels ROM-K1, ROM-K2, ROM-K3, ROM-K4, ROM-K5 and ROM-K6
, potassium inwardly-rectifying channel J1
, ATP-sensitive inward rectifier potassium channel 1
, ATP-sensitive inward rectifier potassium channel 1-like
, potassium inwardly-rectifying channel, subfamily J, member 15
, ATP-regulated potassium channel ROM-K
, inward rectifier K(+) channel Kir1.1
, inwardly rectifying K+ channel
, potassium channel, inwardly rectifying subfamily J member 1
, K+ channel protein
, Potassium inwardly-rectifying channel subfamily J
, inwardly rectifying potassium channel ROMK-2