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Loss of MYO5B in mice recapitulates Microvillus Inclusion Disease and reveals an apical trafficking pathway distinct to neonatal duodenum.
Weis VG
Cellular and molecular gastroenterology and hepatology, 2(2), 131-157 (2016)
An overview and online
registry of microvillus
inclusion disease patients
and their MYO5B mutations
van der Velde KJ
Human Mutation, 34(12), 1597-1605 (2013)
A Rab11a-Rab8a-Myo5B network promotes stretch-regulated exocytosis in bladder umbrella cells.
Khandelwal P
Molecular Biology of the Cell, 24(7), 1007-1019 (2013)
Elisabeth Letellier et al.
British journal of cancer, 117(11), 1689-1701 (2017-10-13)
Selecting the most beneficial treatment regimens for colorectal cancer (CRC) patients remains challenging due to a lack of prognostic markers. Members of the Myosin family, proteins recognised to have a major role in trafficking and polarisation of cells, have recently
Victoria G Weis et al.
Cellular and molecular gastroenterology and hepatology, 2(2), 131-157 (2016-03-29)
Inactivating mutations in MYO5B cause severe neonatal diarrhea in Microvillus Inclusion Disease. Loss of active MYO5B causes the formation of pathognomonic inclusions and aberrations in brush border enzymes. We developed three mouse models of germline, constitutively intestinal targeted and inducible
Inactivation of MYO5B promotes invasion and motility in gastric cancer cells.
Dong W
Digestive Diseases and Sciences, 57(5), 1247-1252 (2012)
Fernando Cartón-García et al.
Scientific reports, 5, 12312-12312 (2015-07-24)
Inherited MYO5B mutations have recently been associated with microvillus inclusion disease (MVID), an autosomal recessive syndrome characterized by intractable, life-threatening, watery diarrhea appearing shortly after birth. Characterization of the molecular mechanisms underlying this disease and development of novel therapeutic approaches
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