Title : High β-glucosidase (GBA) activity not attributable to GBA1 and GBA2 in live normal and enzyme-deficient fibroblasts may emphasise the role of additional GBAs.

Pub. Date : 2015 Nov

PMID : 25996484






4 Functional Relationships(s)
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1 GBA1- and GBA2-deficient genetic conditions, with different phenotypes, are glucosylceramide (GC; the main GBA substrate) accumulating diseases. Glucosylceramides glucosidase, beta, acid Mus musculus
2 GBA1- and GBA2-deficient genetic conditions, with different phenotypes, are glucosylceramide (GC; the main GBA substrate) accumulating diseases. Glucosylceramides glucosidase, beta, acid Mus musculus
3 GBA1- and GBA2-deficient genetic conditions, with different phenotypes, are glucosylceramide (GC; the main GBA substrate) accumulating diseases. Glucosylceramides glucosidase, beta, acid Mus musculus
4 GBA1- and GBA2-deficient genetic conditions, with different phenotypes, are glucosylceramide (GC; the main GBA substrate) accumulating diseases. Glucosylceramides glucosidase, beta, acid Mus musculus