Potassium channel mutant KCNJ5 T158A expression in HAC-15 cells increases aldosterone synthesis. - Wikidata - awgldk - TriplyDB

Potassium channel mutant KCNJ5 T158A expression in HAC-15 cells increases aldosterone synthesis.

Potassium channel mutant KCNJ5 T158A expression in HAC-15 cells increases aldosterone synthesis.

http://www.wikidata.org/entity/Q35872767

about

Intracellular Molecular Differences in Aldosterone- Compared to Cortisol-Secreting Adrenal Cortical Adenomas Genetic alterations in primary aldosteronism Gene mutations that promote adrenal aldosterone production, sodium retention, and hypertension Somatic mutations of the ATP1A1 gene and aldosterone-producing adenomas Genetics of Aldosterone-Producing Adenoma in Korean Patients Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney.Small-Conductance Ca2+-Activated Potassium Channels Negatively Regulate Aldosterone Secretion in Human Adrenocortical Cells.Minireview: aldosterone biosynthesis: electrically gated for our protection Autoimmune mechanisms activating the angiotensin AT1 receptor in 'primary' aldosteronism.Overview of the genetic determinants of primary aldosteronism.Minireview: potassium channels and aldosterone dysregulation: is primary aldosteronism a potassium channelopathy?A novel KCNJ5-insT149 somatic mutation close to, but outside, the selectivity filter causes resistant hypertension by loss of selectivity for potassium Ion channel associated diseases: overview of molecular mechanisms Comprehensive re-sequencing of adrenal aldosterone producing lesions reveal three somatic mutations near the KCNJ5 potassium channel selectivity filter.Understanding primary aldosteronism: impact of next generation sequencing and expression profiling.Prevalence of angiotensin II type 1 receptor (AT1R)-activating autoantibodies in primary aldosteronism Two-pore domain potassium channels in the adrenal cortex.Molecular and Cellular Mechanisms of Aldosterone Producing Adenoma Development Aldosterone-stimulating somatic gene mutations are common in normal adrenal glands Different Somatic Mutations in Multinodular Adrenals With Aldosterone-Producing Adenoma.The potassium channel, Kir3.4 participates in angiotensin II-stimulated aldosterone production by a human adrenocortical cell line Angiotensin II and III metabolism and effects on steroid production in the HAC15 human adrenocortical cell line 3β-Hydroxysteroid dehydrogenase isoforms in human aldosterone-producing adenoma.Gonadotropin-Releasing Hormone Stimulate Aldosterone Production in a Subset of Aldosterone-Producing Adenoma.Novel somatic mutations in primary hyperaldosteronism are related to the clinical, radiological and pathological phenotype Mutated KCNJ5 activates the acute and chronic regulatory steps in aldosterone production a Novel Y152C KCNJ5 mutation responsible for familial hyperaldosteronism type III.Primary aldosteronism: a channelopathy?Role of KCNJ5 in familial and sporadic primary aldosteronism.Regulation of aldosterone biosynthesis by the Kir3.4 (KCNJ5) potassium channel.Steroidogenesis-adrenal cell signal transduction.Regulation of aldosterone synthesis and secretion.Hypomethylation of CYP11B2 in Aldosterone-Producing Adenoma.YPEL4 modulates HAC15 adrenal cell proliferation and is associated with tumor diameter Genetics of adrenocortical tumours.Immunohistochemistry of aldosterone synthase leads the way to the pathogenesis of primary aldosteronism.Of channels and pumps: different ways to boost the aldosterone?Macrolides selectively inhibit mutant KCNJ5 potassium channels that cause aldosterone-producing adenoma.Cortisol overproduction results from DNA methylation of CYP11B1 in hypercortisolemia Channels and pumps in aldosterone-producing adenomas.

P2860

Q26742189-63FA6EB5-A01A-40EF-A525-338D4905832E Q26998759-98A51955-2E1A-4F4A-B540-DE690DDF1423 Q26998925-E1DA373A-CD18-460F-8C07-43D9B7D4B01D Q27007769-DCCF7051-7663-4312-88E4-9C5AFEAF4AA2 Q28552834-B3FF5D61-4765-41F2-A4C7-E7A8B09BEC64 Q30248429-C219D95F-EB9A-43A9-8BCA-29468DF744A1 Q30276331-F45D32F6-8FB4-4C99-86F4-9ADAF8CE42E2 Q30417879-038D2A1E-382C-4FF2-AD80-91F565B76D99 Q33568986-06B52B47-096E-4E0C-A246-155B71143EB8 Q33575337-97CEECCC-B0EE-4DE0-9A0E-43FB0FFCAEF0 Q33585059-0ECF2304-34C8-44C4-82B8-3C53E0E7D1A9 Q34130908-4E0426A1-4121-45E8-A54E-D20F437DE352 Q34311621-C2E41019-8404-4CEB-A4A1-C63625C83345 Q34359244-8D487AD2-F471-4D1D-A610-2EACC40661A5 Q34850075-5258CDAB-20F2-4059-B2EB-98A371453C9A Q35040206-FB705CE2-5641-467C-BD22-B658FA48F5F4 Q35597757-75D56E2C-3705-4E81-9F90-BB4F2E8EAD52 Q35726125-1FE8975C-F85D-4C03-96D5-2B9C553655BE Q35989831-5C9A10E8-679C-423F-8904-E274FEE8992A Q36143337-0D0CD998-4BF9-4876-BB36-7238B28D9BF1 Q36177385-B3DAAA8C-8533-47F7-87B6-F30C7EE791EE Q36486125-45FDD9B9-BF57-402F-93FB-86AA849321C5 Q36766064-1ABBC2A9-D8A3-4EBF-8231-4ECFA6CDEE5A Q36993109-805302E2-A4A9-4C46-A033-922CFEA6C777 Q37199598-D5937CC6-B1B7-49AB-83E6-88EA609AD910 Q37265290-35A640F3-9407-4E49-8730-6E1F16A0A9DD Q37275979-8C14C4DB-7A40-4026-83AE-91FE8E68B94B Q37688189-A0A2529E-2154-465C-995F-CC3EF77A5AFC Q38066356-C41E81A6-8D3F-4A9E-A1F1-F4DDB4853922 Q38119507-AB326192-CC3D-4D2A-AF94-567053611B9C Q38221447-5AD4D715-F462-4720-BDC9-9425E9285385 Q38221449-9502F0E0-D1BF-4419-95D6-FFDA560D567A Q38740220-D56EE1F7-321C-4026-9553-9EC55863AB00 Q38762788-BB8CD699-05FB-4959-8A3B-C7D51481F9C0 Q38793396-88F45231-7D79-4819-95AE-1CF18ABA8308 Q38983295-C30B2F8A-F32F-46D2-AEA4-52B025958DD1 Q39013180-88460399-87A3-4CB4-AB31-C0F3516A0EE3 Q40176652-4D665D20-2CF3-4F79-96A9-E70D79E5D205 Q41318904-67D17308-7DBB-40C9-9E3F-AFA38829CC51 Q42380819-BEADCFD0-8A2A-42D0-9A8A-B8DD398E1495

P2860

Potassium channel mutant KCNJ5 T158A expression in HAC-15 cells increases aldosterone synthesis.

http://www.wikidata.org/entity/Q35872767

description

2012 nî lūn-bûn

@nan

2012年の論文

@ja

2012年論文

@yue

2012年論文

@zh-hant

2012年論文

@zh-hk

2012年論文

@zh-mo

2012年論文

@zh-tw

2012年论文

@wuu

2012年论文

@zh

2012年论文

@zh-cn

name

Potassium channel mutant KCNJ5 ...... creases aldosterone synthesis.

@ast

Potassium channel mutant KCNJ5 ...... creases aldosterone synthesis.

@en

type

label

Potassium channel mutant KCNJ5 ...... creases aldosterone synthesis.

@ast

Potassium channel mutant KCNJ5 ...... creases aldosterone synthesis.

@en

prefLabel

Potassium channel mutant KCNJ5 ...... creases aldosterone synthesis.

@ast

Potassium channel mutant KCNJ5 ...... creases aldosterone synthesis.

@en

P1433

Q35872767-FF81ED47-5C1A-4042-8DA4-44B7665F6A84

P1476

Q35872767-126B94FA-DFEB-40EE-BEC5-3477EAE53B91

P2093

Q35872767-19370CA7-35CA-46DA-8060-80D9DA7893BD

Q35872767-5A90B05F-2454-4FAA-B0F8-C7F4CE1AAEFD

Q35872767-5DD6FAE4-AAC7-40FA-86C8-518F80732F20

Q35872767-903BE859-67E7-421F-BC1E-B86FF92BFECD

Q35872767-947208B8-3982-4D15-94E1-C7A7B36B35E5

P2860

Q35872767-02E54448-4E83-4AC5-847C-6640C566124C

Q35872767-16EF49E4-B169-4E88-8DC8-8F27058DFF46

Q35872767-18CE2647-03DB-4836-ABC3-811974DA6A97

Q35872767-1A1BE5EA-416E-4CB5-86FC-191CE778914A

Q35872767-1C7E81B5-714F-4508-A639-F06A102B4F7F

Q35872767-2810C5CD-C4F0-4CD2-86F0-5BA560B7B673

Q35872767-2E819280-A861-4B9E-B0C5-0A531203D369

Q35872767-2F9F649D-D431-445E-A5D3-A3C6F9B8FDA4

Q35872767-35A57327-2EA4-423D-8C5E-5A5A52F48B8E

Q35872767-3D9E56C6-0121-4CEB-AE66-58B99332059E

P304

Q35872767-207382F4-E11F-4C39-9F1C-6BDB0880B86F

P31

Q35872767-69158EB2-28EA-413E-BFD8-C38CCEA8092D

P356

Q35872767-CC0788DC-38DD-4ABA-BA13-EE937DE28D87

P407

Q35872767-723C0BEB-A306-4491-AB2A-5EB9625A8EA6

P433

Q35872767-3DFA6FEF-EC77-46BD-AD43-55DAF9BACFD5

P478

Q35872767-0BEEBE56-AF35-4975-84BE-8AC29AA9F28E

P577

Q35872767-1B237411-BCC1-4052-A0B0-BCA6DF0D2AEA

P5875

Q35872767-C96126C7-CDA2-432A-8AB4-C9E5618BC739

P698

Q35872767-012CB255-B119-4D98-AD4C-2D28B86E63CF

P932

Q35872767-B51A100B-5D70-4040-B5FC-5ABA1DCF4B92

P356

P1433

P1476

Potassium channel mutant KCNJ5 ...... creases aldosterone synthesis.

@en

P2093

Celso E Gomez-Sanchez

http://www.w3.org/2001/XMLSchema#string

Elise P Gomez-Sanchez

http://www.w3.org/2001/XMLSchema#string

Kenji Oki

http://www.w3.org/2001/XMLSchema#string

Maria W Plonczynski

http://www.w3.org/2001/XMLSchema#string

Milay Luis Lam

http://www.w3.org/2001/XMLSchema#string

P2860

Glucocorticoid-suppressible hyperaldosteronism results from hybrid genes created by unequal crossovers between CYP11B1 and CYP11B2

Crystal Structure of the Eukaryotic Strong Inward-Rectifier K+ Channel Kir2.2 at 3.1 A Resolution

Hereditary hypertension caused by chimaeric gene duplications and ectopic expression of aldosterone synthase

Calmodulin-dependent kinase I regulates adrenal cell expression of aldosterone synthase

Further evidence for linkage of familial hyperaldosteronism type II at chromosome 7p22 in Italian as well as Australian and South American families

TASK channel deletion in mice causes primary hyperaldosteronism.

Molecular basis for the modulation of native T-type Ca2+ channels in vivo by Ca2+/calmodulin-dependent protein kinase II.

Full deacylation of polyethylenimine dramatically boosts its gene delivery efficiency and specificity to mouse lung.

Expression of a constitutive form of calcium/calmodulin dependent protein kinase II leads to arrest of the cell cycle in G2

A public genome-scale lentiviral expression library of human ORFs.

P304

1774-1782

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1210/EN.2011-1733

http://www.w3.org/2001/XMLSchema#string

P407

P433

4

http://www.w3.org/2001/XMLSchema#string

P478

153

http://www.w3.org/2001/XMLSchema#string

P577

2012-02-07T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P5875

221815606

http://www.w3.org/2001/XMLSchema#string

P698

22315453

http://www.w3.org/2001/XMLSchema#string

P932

3320257

http://www.w3.org/2001/XMLSchema#string