Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 Proteins (KCNJ1)

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 (96) and and many more products for this protein.

list all proteins Gene Name GeneID UniProt
KCNJ1 3758 P48048
Rat KCNJ1 KCNJ1 24521 P35560
KCNJ1 56379 O88335
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Top Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 Proteins at antibodies-online.com

Showing 7 out of 8 products:

Catalog No. Origin Source Conjugate Images Quantity Delivery Price Details
Escherichia coli (E. coli) Human His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg 30 to 35 Days
$5,370.21
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Insect Cells Human rho-1D4 tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 0.5 mg 50 to 55 Days
$7,493.38
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Insect Cells Mouse rho-1D4 tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 0.25 mg 50 to 55 Days
$5,262.31
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Escherichia coli (E. coli) Mouse His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg 30 to 35 Days
$5,370.21
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Escherichia coli (E. coli) Human His tag 100 μg 11 Days
$356.40
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Yeast Human His tag 100 μg 8 to 11 Days
$429.00
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Wheat germ Human GST tag 2 μg 11 to 12 Days
$338.33
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KCNJ1 Proteins by Origin and Source

Origin Expressed in Conjugate
Human , , ,
, ,
Mouse (Murine) ,
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More Proteins for Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 (KCNJ1) Interaction Partners

Human Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 (KCNJ1) interaction partners

  1. endosomal trafficking factors CORVET and ESCRT suppress plasma membrane residence of the renal outer medullary potassium channel

  2. We replicated the methods in a previous study to detect rare and potentially loss-of-function variants in SLC12A3, SLC12A1, and KCNJ1 reducing blood pressure in variant carriers as compared with noncarriers using whole exome sequencing data. Our study confirmed that SLC12A3, SLC12A1, and KCNJ1 are indeed genes protective of hypertension in the general population.

  3. The presence of ROMK protein was observed in the inner mitochondrial membrane fraction. Moreover, colocalization of the ROMK protein and a mitochondrial marker in the mitochondria of fibroblast cells was shown by immunofluorescence.

  4. 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)

  5. WNK4 is a substrate of SFKs and the association of c-Src and PTP-1D with WNK4 at Tyr(1092) and Tyr(1143) plays an important role in modulating the inhibitory effect of WNK4 on ROMK

  6. knockdown of KCNJ1 in HK-2 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

  7. The association between polymorphisms in KCNJ1, SLC12A1, and 7 other genes and calcium intake and colorectal neoplasia risk was studied.

  8. A KCNJ1 SNP was associated with increased FG during HCTZ treatment.

  9. 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.

  10. Findings suggest that 11q24 is a susceptible locus for openness, with KCNJ1 as the possible candidate gene.

  11. no mutation in the KCNJ1 gene, among patients suffering from bartter and Gitelman syndromes

  12. PI3K-activating hormones inhibit ROMK by enhancing its endocytosis via a mechanism that involves phosphorylation of WNK1 by Akt1 and SGK1.

  13. THGP modulation of ROMK function confers a new role of THGP on renal ion transport and may contribute to salt wasting observed in FJHN/MCKD-2/GCKD patients.

  14. KCNJ1 mutations are associated with Bartter syndrome.

  15. ROMK1 is a substrate of PKC and that serine residues 4 and 201 are the two main PKC phosphorylation sites that are essential for the expression of ROMK1 in the cell surface

  16. One disease-causing mutation in the ROMK channel truncates the extreme COOH-terminus and induces a closed gating conformation.

  17. In a heterozgous Bartter syndrome patient, AA exchanges Arg338Stop & Met357Thr in ROMK exon 5 alter the C-terminus of the ROMK protein & can affect channel function.

  18. Findings support the proposed role of ROMK channels in potassium recycling and in the regulation of K+ secretion and present a rationale for the phenotype observed in patients with ROMK deficiency.

  19. NH(2)-terminal phosphorylation modifying a COOH-terminal ER retention signal in ROMK1 could serve as a checkpoint for proper subunit folding critical to channel gating.

  20. ROMK is antagonistically regulated by long and kidney-specific WNK1 isoforms

Cow (Bovine) Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 (KCNJ1) interaction partners

  1. The findings support ROMK as the pore-forming subunit of the cytoprotective mitoK(ATP) channel in heart mitochondria.

Mouse (Murine) Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 (KCNJ1) interaction partners

  1. WNK1, but not WNK4, is required for high potassium intake-induced stimulation of ROMK activity in convoluted kidney tubules.

  2. ROMK is expressed in the urinary tract at both protein and mRNA levels. Significant enlargement and hypertrophy of the bladder may contribute to hydronephrosis in male ROMK KO mice.

  3. The results provide evidence that NHERF1 mediates K(+) current activity through acceleration of the surface expression of ROMK1 K(+) channels in M-1 cells.

  4. ENaC and ROMK channel activity in kidney tubules are inhibited in TgWnk4(pseudoaldosteronism type II) mice. Wnk4(PHAII)-induced inhibition of ENaC and ROMK may contribute to the suppression of K(+) secretion in the tubules.

  5. The differential regulation of ROMK, large-conductance Ca(2+)-activated K(+) (BK) channel, BK-alpha and NKCC2 between female and male mice, at least, were partly mediated via WNK1 pathway, which may contribute to the sexual dimorphism of plasma K(+) and blood pressure control.

  6. Suggest that the hyperkalemia in knock-in mouse with the CUL3(Delta403-459) mutation is not caused by reduced ROMK expression in the distal nephron.

  7. 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.

  8. Lovastatin stimulates ROMK1 channels by inducing PI(4,5)P2 synthesis, suggesting that the drug could reduce cyclosporine-induced nephropathy.

  9. ROMK1 protein abundance and activity are down-regulated by SPAK and OSR1

  10. It was concluded that miR-194 regulates ROMK channel activity by modulating ITSN1 expression thereby enhancing ITSN1/WNK-dependent endocytosis.

  11. THGP modulation of ROMK function confers a new role of THGP on renal ion transport and may contribute to salt wasting observed in FJHN/MCKD-2/GCKD patients.

  12. hypertension resistance sequence variants inhibit ROMK channel function by different mechanisms

  13. knockout mice have impaired renal NaCl absorption; a model for type II Bartter's syndrome

  14. Absence of small conductance K+ channel (SK) activity in apical membranes of thick ascending limb and cortical collecting duct in knockout mice a model for bartter's disease__

  15. SGK-1 phosphorylation of ROMK drives expression on the plasmalemma; because SGK-1 is an early aldosterone-induced gene, results suggest a possible molecular mechanism for aldosterone-dependent regulation of the secretory potassium channel in the kidney

  16. ROMK is required for functional expression of the 70-pS K channel in the thick ascending limb.

  17. mutant WNK4 does not have a dominant effect on the cellular localization of kidney ROMK

  18. The expression of ROMK channels in the plasma membrane is regulated by PTK, SGK, and with-no-lysine-kinase 4. A recent study indicated that ROMK channels can be monoubiquitinated and monoubiquitination regulates the surface expression of ROMK channels.

  19. Potassium absorption in the loop of Henle is reduced in Romk-deficient mice and can account for a significant fraction of renal potassium loss.

  20. mRNA expression of ROMK is augmented in the renal medullary tubule by NaCl-induced hypertonicity through stimulation of ROMK gene transcription, and that TonEBP and the p38 MAPK and ERK pathways are involved in this effect.

Zebrafish Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 (KCNJ1) interaction partners

  1. 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 Inwardly-Rectifying Channel, Subfamily J, Member 1 (KCNJ1) Protein Profile

Protein Summary

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.

Gene names and symbols associated with KCNJ1

  • potassium voltage-gated channel subfamily J member 1 (KCNJ1)
  • potassium voltage-gated channel subfamily J member 1 L homeolog (kcnj1.L)
  • potassium voltage-gated channel subfamily J member 1 (kcnj1)
  • potassium voltage-gated channel subfamily J member 1 (Kcnj1)
  • potassium inwardly-rectifying channel, subfamily J, member 1 (Kcnj1)
  • potassium inwardly-rectifying channel, subfamily J, member 1a, tandem duplicate 1 (kcnj1a.1)
  • Kcnj protein
  • kcnj1 protein
  • Kir1.1 protein
  • ROMK protein
  • romk1 protein
  • Romk2 protein
  • wu:fl37c05 protein
  • zgc:63534 protein

Protein level used designations for KCNJ1

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 , KAB-1 , Potassium inwardly-rectifying channel subfamily J , kir1.1 , inwardly rectifying potassium channel ROMK-2 , LOW QUALITY PROTEIN: ATP-sensitive inward rectifier potassium channel 1

GENE ID SPECIES
3758 Homo sapiens
428236 Gallus gallus
447262 Xenopus laevis
466846 Pan troglodytes
489285 Canis lupus familiaris
539250 Bos taurus
714848 Macaca mulatta
100072580 Equus caballus
100173141 Pongo abelii
100470569 Ailuropoda melanoleuca
100487609 Xenopus (Silurana) tropicalis
100517668 Sus scrofa
100556003 Anolis carolinensis
100579741 Nomascus leucogenys
24521 Rattus norvegicus
56379 Mus musculus
386933 Danio rerio
100722828 Cavia porcellus
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