ライフサイエンスコーパス: maltase

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1 r target antigen excluded megalin, CD10, and maltase.

2 The physiological relevance of acid maltase (acid alpha-glucosidase, an enzyme that degrades

3 simulate these barriers in a villous mucosa, maltase activity (measured in vitro) was distributed ove

4 accharomyces cerevisiae that is deficient in maltase activity and unable to grow using maltose as a c

5 ion of AHA1 enhances induced Mal63-dependent maltase activity levels 2-fold, whereas overproduction o

6 Maltase activity occurred over the pH range 3.5-6.3 with

7 bstrates hydrolysed by the multiple sites of maltase activity.

8 not affect inhibition of alpha-glucosidase (maltase) activity, which remained relatively low but sta

9 Maltase and SGLT1 capacities increased only sublinearly

10 etary composition resulted in an increase in maltase and SGLT1 capacities mediated non-specifically b

11 ncoding the major soluble alpha-glucosidase (maltase) and flanking sequences from Sulfolobus solfatar

12 ors decreased with load: from 6.5 to 2.4 for maltase, and from 1.1 to 0.5 for SGLT1.

13 The levels of sucrase, maltase, and lactase decreased in wild-type mice p.i. wi

14 ALx1 encodes maltose permease, MALx2 encodes maltase, and MALx3 encodes an activator of MALx1 and MAL

15 Activities of lactase, sucrase, maltase, and palatinase consistently exceeded reference

16 haridases [K(i) 0.081 muM for rat intestinal maltase] and is more effective in the suppression of hyp

17 alpha -glucosidase (GAA) (also called "acid maltase"), causes death in early childhood related to gl

18 In late (adult)-onset acid maltase deficiency (glycogen storage disease type II [GS

19 cular atrophy (SMA), and Pompe disease (acid maltase deficiency [AMD]), are candidates for universal

20 hey form long lists for others, such as acid maltase deficiency and myophosphorylase deficiency; and

21 The diagnosis of Pompe disease (acid maltase deficiency, glycogen storage disease type II) in

22 Tissue maltase, diamine oxidase, and ornithine decarboxylase we

23 Maltase expression in strains carrying constitutive and

24 ted disorder caused by mutations in the acid maltase (GAA) gene.

25 Brush-border maltase-glucoamylase (MGA) activity serves as the final

26 o glucose by the mucosal alpha-glucosidases, maltase-glucoamylase (MGAM) and sucrase-isomaltase (SI).

27 including N- and C-terminal subunits of both maltase-glucoamylase and sucrase-isomaltase.

28 hesis, we have cloned human small intestinal maltase-glucoamylase cDNA to permit study of the individ

29 Maltase-glucoamylase cDNA was amplified from human intes

30 Maltase-glucoamylase has two catalytic sites identical t

31 cause of immaturity or malnutrition and that maltase-glucoamylase plays a unique role in the digestio

32 Human maltase-glucoamylase was purified by immunoisolation and

33 l a structural homologue to human intestinal maltase-glucoamylase with a highly conserved catalytic d

34 the mouse intestinal brush-border hydrolase maltase in series with the glucose transporter SGLT1, fo

35 nd hsc82 Delta cpr7 Delta, are defective for maltase induction and exhibit significantly reduced grow

36 aining cis-acting promoter elements from the Maltase-like I (MalI) and Apyrase (Apy) genes were clone

37 The apparently high safety factor for maltase may be related to the multiple natural substrate

38 crease in intestinal mass, without change in maltase or SGLT1 activities per milligram of tissue.

39 mylase), beta-amylase, starch phosphorylase, maltase, pullulanase or D-enzyme could be detected in cr

40 ting enzyme; DPE2), a protein similar to the maltase Q (MalQ) gene product involved in maltose metabo

41 ructural genes encoding maltose permease and maltase requires the MAL activator, a DNA-binding transc

42 ies of debranching enzyme and lysosomal acid maltase, two major hepatic alpha-glucosidases, were unal

43 al glycogen storage disease with normal acid maltase" which was originally described by Danon et al.,

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