ライフサイエンスコーパス: Liddle's syndrome

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1 , causing an inherited form of hypertension (Liddle's syndrome).

2 s, including a genetic form of hypertension (Liddle's syndrome).

3 nts could provide a simple clinical test for Liddle's syndrome.

4 lso contribute to excessive Na+ transport in Liddle's syndrome.

5 tion of increased sodium channel activity in Liddle's syndrome.

6 r of channels in the plasma membrane seen in Liddle's syndrome.

7 In Liddle's syndrome, a rare inherited form of hypertension

8 tes derived from an individual affected with Liddle's syndrome, an autosomal dominant form of human h

9 Mutations in this PPXY domain cause Liddle's syndrome, an autosomal dominant, salt-sensitive

10 Liddle's syndrome, an inherited form of hypertension, is

11 Liddle's syndrome, an inherited form of hypertension, is

12 units increase renal Na+ absorption, causing Liddle's syndrome, an inherited form of hypertension.

13 ction may play a role in the pathogenesis of Liddle's syndrome and other forms of hypertension.

14 cocorticoid-suppressible hyperaldosteronism, Liddle's syndrome, and apparent mineralocorticoid excess

15 These results strongly suggest that PHA1 and Liddle's syndrome are allelic variants caused by mutatio

16 iated with diseases like cystic fibrosis and Liddle's syndrome are irreversibly stimulated by membran

17 Liddle's syndrome-associated mutations that prevent the

18 A mutation associated with Liddle's syndrome (betaR566X) abolished the effect of Ne

19 lucocorticoid-suppressible aldosteronism and Liddle's syndrome, each inherited as an autosomal-domina

20 ma membrane or to the hypertensive disorder, Liddle's syndrome, in which channel residency time at th

21 Liddle's syndrome is a rare inherited form of hypertensi

22 Liddle's syndrome is caused by an activating mutation in

23 urface but also provide a mechanism by which Liddle's syndrome mutations alter ENaC activity.

24 Here, we found that Liddle's syndrome mutations have two distinct effects of

25 Liddle's syndrome of hypertension and pseudoaldosteronis

26 eta-subunit mutation, R564X, associated with Liddle's syndrome, open probability in both high- and lo

27 r excess, termed pseudohypoaldosteronism and Liddle's syndrome, respectively.

28 uence is the target for mutations that cause Liddle's syndrome, suggesting that cAMP-mediated translo

29 s) in three brothers with genetically proven Liddle's syndrome, their unaffected sister, and 40 normo

30 Moreover, expression of a Liddle's syndrome-type beta-mENaC mutant (Y618A) greatly

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