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2 ace damage that phenocopied aspects of human pseudohypoaldosteronism-1 MG disease and was sex depende
3 neralocorticoid deficiency or excess, termed pseudohypoaldosteronism and Liddle's syndrome, respectiv
4 ation in the CD and demonstrated features of pseudohypoaldosteronism, including hyperkalemia, hyperal
9 epithelial Na(+) channel (ENaC) containing a pseudohypoaldosteronism type 1 (PHA-1)-causing missense
12 cient mice is similar to that of humans with pseudohypoaldosteronism type 1 and may provide a useful
13 unction leads to severe disorders, including pseudohypoaldosteronism type 1 and respiratory distress.
15 ia and hyponatremia from autosomal recessive pseudohypoaldosteronism type 1 requiring aggressive ther
16 urface epithelium, leading to colon-specific pseudohypoaldosteronism type 1 with mineralocorticoid re
17 on is associated with respiratory disorders, pseudohypoaldosteronism type 1, and Liddle syndrome.
18 o adverse cardiovascular outcome occurred in pseudohypoaldosteronism type 1, but rather an improved d
19 n of a ubiquitous long WNK1 transcript cause pseudohypoaldosteronism type 2 (PHA II), characterized b
20 ns of 2 family members, WNK1 and WNK4, cause pseudohypoaldosteronism type 2 (PHA2), an autosomal-domi
23 of WNK1 that increase WNK1 transcript cause pseudohypoaldosteronism type 2, an autosomal-dominant di
25 notypes dominated by renal disease (systemic pseudohypoaldosteronism type I and Liddle syndrome).
26 ubunits can lead to the salt wasting disease pseudohypoaldosteronism type I, associated with decrease
27 tion in alleviating human disease, including pseudohypoaldosteronism type I, hypotension, and neonata
28 ating that leads to the salt-wasting disease pseudohypoaldosteronism type I, was rescued by S3969.
32 work has shown that mutations in WNK4 cause pseudohypoaldosteronism type II (PHAII), a disease featu
35 lysine (K) at a key catalytic residue] cause pseudohypoaldosteronism type II (PHAII), a Mendelian dis
37 s in the gene encoding the kinase WNK4 cause pseudohypoaldosteronism type II (PHAII), a syndrome feat
38 e kinases, have recently been shown to cause pseudohypoaldosteronism type II (PHAII), an autosomal do
41 butes to the pathogenesis of hypertension in pseudohypoaldosteronism type II caused by WNK1 and, poss
44 xcessive sodium retention, and hypertension (pseudohypoaldosteronism type II or Gordon's syndrome).
45 ene result in its overexpression and lead to pseudohypoaldosteronism type II, a disease with salt-sen
46 e the expression of WNK1 in humans and cause pseudohypoaldosteronism type II, a form of hypertension.
47 ine kinase WNK4 [with no lysine (K) 4] cause pseudohypoaldosteronism type II, a Mendelian disease fea
49 o its overexpression and are responsible for pseudohypoaldosteronism type II, an autosomal dominant d
50 The discovery of four genes responsible for pseudohypoaldosteronism type II, or familial hyperkalemi
51 g WNK4, cause hypertension and hyperkalemia (pseudohypoaldosteronism type II, PHAII) by altering rena
55 mately 2.0% per minute) reported in systemic pseudohypoaldosteronism, which has loss-of-function muta