ライフサイエンスコーパス: dysgenic

1 Deletion mutants were expressed in dysgenic alpha(1S)-null myotubes and analyzed by voltage

2 these constructs in dyspedic (RyR1 null) and dysgenic (alpha(1S) null) myotubes was used to test for

3 pecific arrangement of DHPRs was examined in dysgenic (alpha(1S)-null) myotubes reconstituted with di

4 domain (alpha1S 701-1873) were expressed in dysgenic alpha1S-null myotubes.

5 N- and C-terminal domains were evaluated in dysgenic (alpha1S-null) myotubes for phenotypic expressi

6 Upon expression in beta1-null or dysgenic (alpha1S-null) myotubes, punctate avidin fluore

7 Expressed in dysgenic (alpha1S-null) myotubes, YFP-beta1a-CFP and CFP

8 iency was similar after expression in either dysgenic (alpha1S-null) or dyspedic (RyR1-null) myotubes

9 the gonad and that mutant gonads are highly dysgenic and possibly feminized.

10 positive potentials (DeltaF/Fmax) in double dysgenic/beta1 KO myotubes overexpressing the pore mutan

11 quences of this mutation, we expressed it in dysgenic (Ca(V)1.1 null) myotubes.

12 Dysgenic Ca2+ channels may be a minor component of this

13 han the single-channel current estimated for dysgenic Ca2+ channels, which was 84 +/- 9 fA under the

14 dulators on whole-cell current properties in dysgenic (CaV1.1-null) myotubes reconstituted with eithe

15 stle number that had been started from a P-M dysgenic cross.

16 in hybrid dysgenesis; in particular, certain dysgenic crosses in Drosophila virilis result in mobiliz

17 oming increasingly genetic in nature or that dysgenic dynamics have accelerated.

18 induction of a 2.6-kb RNA in the ovaries of dysgenic females that is expressed at very low levels in

19 Similar to primary cultures, dysgenic (GLT) myoblasts show a higher incidence of cell

20 As dysgenic hybrids age, however, fertility is restored, P

21 s of Notch signaling leads to formation of a dysgenic lens, which in loss-of-function mice undergoes

22 d as GFP fluorescence in the live progeny of dysgenic males.

23 using cell lines (GLT and NLT) derived from dysgenic (mdg/mdg) and normal (+/+) muscle, respectively

24 beta 1 subunit is localized appropriately in dysgenic, mdg/mdg, (alpha 1s-null) cells.

25 t of Idys, the Ca2+ current of myotubes from dysgenic mice lacking the skeletal DHPR alpha1S subunit

26 However, paralytic, muscular dysgenic mutant chick embryos also exhibit significant i

27 a1S C-terminal was inaccessible to avidin in dysgenic myotubes (containing RyR1).

28 When expressed in dysgenic myotubes (which lack endogenous alpha(1S)), alp

29 ving this signal from RyR-1, we expressed in dysgenic myotubes a chimera (SkLC) having skeletal (Sk)

30 f either P/Q-type or N-type Ca2+ channels in dysgenic myotubes does not result in electrically evoked

31 Dysgenic myotubes expressing GFP-alpha(1S)[III-IVa] yiel

32 Dysgenic myotubes expressing GFP-SkLC or SkLC lacked EC

33 expression of GFP-alpha1S and GFP-alpha1C in dysgenic myotubes restored skeletal- and cardiac-type ex

34 xpression of cardiac L-type Ca2+ channels in dysgenic myotubes results in large Ca2+ currents and ele

35 keletal muscle-type ryanodine receptor 1 and dysgenic myotubes that lack the dihydropyridine receptor

36 1S in beta1-null myotubes and its absence in dysgenic myotubes was confirmed by immunofluorescence la

37 Dysgenic myotubes were injected with cDNA encoding green

38 In dysgenic myotubes, energy transfer was observed from an

39 However, compared with dysgenic myotubes, the FRET efficiency in dyspedic myotu

40 and expressed each of the fusion channels in dysgenic myotubes.

41 Here we use WT and Ca(V)1.1 null (dysgenic) myotubes to provide evidence for an unexplored

42 fter coexpression with unlabeled alpha1S (in dysgenic or beta1-null myotubes), both constructs produc

43 han direct observations suggest, because the dysgenic population consequences of a biased sex ratio a

44 question of whether the lack of the DHPR in dysgenic skeletal muscle results in a failure of triad f

45 Dmrt1 null mutant mice have severely dysgenic testes in which Sertoli cells and germ cells bo

46 tions of Wt1-/- cells showed hypoplastic and dysgenic testes, with seminiferous tubules lacking sperm

47 that Ca(2+) sparks are not more frequent in dysgenic than in WT myotubes adds support to the hypothe

48 ce responsible for the mutant phenotype of a dysgenic yellow allele has been characterized and named