1                                              MEB represented approximately 5% of all enterococcal bac

2 ockout HEK293T cells and fibroblasts from an MEB patient to gain deeper insight into the molecular ch

3      Mutations reported in genes of FCMD and MEB patients suggest that the genes may be involved in p

4 ion (heterogeneous) enterococcal bacteremia (MEB) is rarely reported.

5                        Here we show, in both MEB and FCMD patients, that alpha-dystroglycan is expres

6 ainly been associated with muscle-eye-brain (MEB) disease.

7 h mutations in POMT2 had a Muscle-Eye-Brain (MEB)-like condition.

8  to detect this subpopulation and determined MEB frequency.

9                    Muscle eye brain disease (MEB) and Fukuyama congenital muscular dystrophy (FCMD) a

10 that patients with muscle-eye-brain disease (MEB) and Fukuyama congenital muscular dystrophy (FCMD),

11  dystrophy (FCMD), Muscle-Eye-Brain disease (MEB) and Walker-Warburg syndrome (WWS), which are associ

12 Syndrome (WWS) and muscle-eye-brain disease (MEB) are caused by mutations in two genes involved in O-

13  dystrophy (FCMD), muscle-eye-brain disease (MEB), and Walker-Warburg syndrome are congenital muscula

14                    Muscle-eye-brain disease (MEB), is caused by mutations in the POMGnT1 gene.

15 gs further define the phenotypic spectrum of MEB and its occurrence in the US population.

16 ntribute to the complex clinical symptoms of MEB or a-dystroglycanopathy in general and suggests that

17 th fringe-like glycosyltransferases, and the MEB gene, POMGnT1, seems to be a new glycosyltransferase

18 tween these models, we compared rafts in the MEB-4 melanoma cell line and its GSL-deficient derivativ

19 hat is similar to that seen in patients with MEB and FCMD.

20                                         WWS, MEB, FCMD and the myd mouse are also associated with neu

21 rmalities with striking similarities to WWS, MEB, FCMD and the myd mouse.