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1 cell mass and function: the focal variant of congenital hyperinsulinism.
2 ium channel Kir6.2, respectively, results in congenital hyperinsulinism.
3 utant KATP channels previously identified in congenital hyperinsulinism.
4 surface lead to loss of channel function and congenital hyperinsulinism.
5 They represent a novel cause of focal congenital hyperinsulinism.
6 ssense Kir6.2 mutation, G156R, identified in congenital hyperinsulinism.
7 sible for the most common and severe form of congenital hyperinsulinism.
8 imination between focal and diffuse forms of congenital hyperinsulinism.
9 sults in loss of channel function as seen in congenital hyperinsulinism.
10 subunit of the channel, is a major cause of congenital hyperinsulinism.
11 A116P and V187D, identified in patients with congenital hyperinsulinism.
12 ly prevent cell surface expression and cause congenital hyperinsulinism.
13 nfants and children seen in the rare disease congenital hyperinsulinism.
14 cells, thereby causing insulin secretion and congenital hyperinsulinism.
15 regions to discover new molecular causes of congenital hyperinsulinism.
16 iabetes, whereas increased K(D) values cause congenital hyperinsulinism.
17 hanism for loss of KATP channel function and congenital hyperinsulinism and support the importance of
18 Thus, sulfonylureas may be used to treat congenital hyperinsulinism caused by certain K(ATP) chan
22 K(ATP) channel trafficking defects underlie congenital hyperinsulinism (CHI) cases unresponsive to t
30 rgery with curative intent can be offered to congenital hyperinsulinism (CHI) patients, provided that
31 ory subunit, sulfonylurea receptor 1, causes congenital hyperinsulinism (CHI), a neonatal disease cha
32 cal excitability and secretion, resulting in congenital hyperinsulinism (CHI), whereas gain-of-functi
35 f glutamate dehydrogenase (GDH) in a form of congenital hyperinsulinism (GDH-HI) is providing a model
36 cation to treat nesidioblastosis and diffuse congenital hyperinsulinism has varying efficacy and caus
38 on and severe form of diazoxide-unresponsive congenital hyperinsulinism (HI) require a pancreatectomy
40 icacy of this form of linkage-mapping, using congenital hyperinsulinism (HI), an autosomal recessive
48 reatment of insulinomas and focal lesions in congenital hyperinsulinism is invasive and carries major
52 evere recessively inherited diffuse forms of congenital hyperinsulinism or, when associated with loss
56 hannels with reduced activity are a cause of congenital hyperinsulinism, whereas hyperactive channels
57 annel function are typically associated with congenital hyperinsulinism, whereas those that increase