ライフサイエンスコーパス: maltase

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 Mixed-type inhibition on rat maltase activity was observed.

8 bstrates hydrolysed by the multiple sites of maltase activity.

9 duced a synergistic inhibitory effect on rat maltase activity.

10 The opposite was observed on maltase activity.

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

12 a extracts were very effective in inhibiting maltase and glucoamylase activity, but only white tea ex

13 Maltase and SGLT1 capacities increased only sublinearly

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

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

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

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

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

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

20 ays tested for activity of lactase, sucrase, maltase, and palatinase.

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

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

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

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

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

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

27 Tissue maltase, diamine oxidase, and ornithine decarboxylase we

28 Maltase expression in strains carrying constitutive and

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

30 man bile salt activated lipase (hBAL); human maltase-glucoamylase (hMGA); human pancreatic alpha-amyl

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

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

33 e (AMY1), pancreatic amylase (AMY2A, AMY2B), maltase-glucoamylase (MGAM), and sucrase-isomaltase (SI)

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

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

36 Maltase-glucoamylase cDNA was amplified from human intes

37 Maltase-glucoamylase has two catalytic sites identical t

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

39 Human maltase-glucoamylase was purified by immunoisolation and

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

41 owest free energy values for enzymes DPP-IV, maltase-glucoamylase, pancreatic alpha-amylase and sucra

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

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

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

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

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

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

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

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

50 Inhibition of maltase, sucrase, isomaltase and glucoamylase activity b

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

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