ライフサイエンスコーパス: posterior limb

1 Hedgehog-dependent growth directed from the posterior limb.

2 xD genomic region specifically in the distal posterior limb.

3 and become the bone, muscle, and skin of the posterior limb.

4 that Shh no longer maintains Gremlin in the posterior limb.

5 g the spatial expression of Hox genes in the posterior limb and regulating ZPA function, Pbx1/Pbx2 ex

6 ; overlapping regions were found in the left posterior limb and the retrolenticular part of internal

7 apsule (SMA in anterior limb and genu; M1 in posterior limb) and traverse the midsection of the cereb

8 ssed in the pre-limb lateral plate mesoderm, posterior limb bud and flank mesenchyme, a pattern remin

9 come to occupy their normal positions in the posterior limb bud during development are not understood

10 precise restriction of Shh expression to the posterior limb bud is essential for its polarizing effec

11 program that restricts ZPA formation to the posterior limb bud mesenchyme.

12 ild-type mouse limb bud, the Shh(-/-) mutant posterior limb bud mesoderm does not cause digit duplica

13 The zone of polarizing activity (ZPA) in the posterior limb bud produces Sonic Hedgehog (Shh) protein

14 hog (Shh) is a secreted molecule made in the posterior limb bud that affects patterning and developme

15 are known to restrict Shh expression to the posterior limb bud, how they function together remains u

16 ed from the critical signaling center of the posterior limb bud, the Zone of Polarizing Activity (ZPA

17 rafts of extracellular matrix from the Mouse Posterior Limb Bud-4 cell line can induce supernumerary

18 h, is known to promote Shh expression in the posterior limb bud.

19 romatin decompaction over HoxD in the distal posterior limb compared with anterior.

20 required for the expression of Hand2 in the posterior limb field.

21 cally begins with a power-stroke by the most posterior limbs, followed progressively by power-strokes

22 through the genu and anterior portion of the posterior limb (ICp).

23 We find that the posterior limb is refractory to Gremlin induction in res

24 uarter-period phase difference with the more posterior limbs leading the cycle.

25 of polarizing activity (ZPA) located at the posterior limb margin.

26 ors are indeed expressed at the anterior and posterior limb margins over a wide range of limb bud sta

27 ient for Tbx2 expression at the anterior and posterior limb margins.

28 Later ablation of T-box3 in posterior limb mesenchyme causes digit loss.

29 Our results show that all posterior limb mesenchyme cells, as well as the ectoderm

30 direct expression of a reporter gene in the posterior limb mesenchyme.

31 ver, once the ZPA has become established the posterior limb mesoderm displays resistance to the induc

32 rest: splenium of corpus callosum (SPCC) and posterior limb of internal capsule (PLIC).

33 of internal capsule, 130 x 10(-5) mm(2)/sec; posterior limb of internal capsule, 109 x 10(-5) mm(2)/s

34 ala (SLEA, 86%), interstitial nucleus of the posterior limb of the anterior commissure (IPAC, 56%), b

35 tria terminalis, interstitial nucleus of the posterior limb of the anterior commissure and central an

36 ular EA, and the interstitial nucleus of the posterior limb of the anterior commissure frequently and

37 tended amygdala, interstitial nucleus of the posterior limb of the anterior commissure nucleus, and b

38 entral and anterior/dorsal banks of a dorsal/posterior limb of the inferior temporal sulcus, similar

39 tter (0.30, 0.12-0.77; p=0.01), and abnormal posterior limb of the internal capsule (0.38, 0.17-0.85;

40 ng white matter (NAWM) and the contralateral posterior limb of the internal capsule (PLIC) after age

41 zation of corticospinal tracts (CSTs) in the posterior limb of the internal capsule (PLIC).

42 fference -0.01, 95% CI -0.03 to 0.02) in the posterior limb of the internal capsule between the two g

43 Myelination of the posterior limb of the internal capsule was less develope

44 tion in the ipsilateral external capsule and posterior limb of the internal capsule, and corona radia

45 pinal tract in the centrum semiovale, in the posterior limb of the internal capsule, and in the cereb

46 rain size, less-developed myelination of the posterior limb of the internal capsule, and more immatur

47 ferent from those of control subjects in the posterior limb of the internal capsule, corona radiata,

48 ral structures, degree of myelination in the posterior limb of the internal capsule, gyral maturation

49 nd in preserved fractional anisotropy in the posterior limb of the internal capsule, measured with ma

50 normalities and diffusion restriction in the posterior limb of the internal capsule, often also optic

51 n, in the parenchyma and vessel walls of the posterior limb of the internal capsule, putamen, globus

52 d splenium of the corpus callosum, the right posterior limb of the internal capsule, right external c

53 minantly in the periventricular regions, the posterior limb of the internal capsule, the external cap

54 a radiata, anterior thalamic radiations, and posterior limb of the internal capsule.

55 tracts studied (P, <.001 to <.03) except the posterior limb of the internal capsule.

56 he thalami, putamen, occipital cortices, and posterior limb of the internal capsules after TBI.

57 FA of the posterior limb of the left internal capsule was positive

58 Because the posterior limb of the rostral suprasylvian sulcus (RSp)

59 the corpus callosum, bilateral anterior and posterior limbs of internal capsule, bilateral retrolent

60 ons: the cerebral peduncle, the anterior and posterior limbs of the internal capsule (ALIC and PLIC),

61 ) and splenium of the corpus callosum (SCC), posterior limbs of the internal capsules (PLIC), superio

62 ation, and fractional anisotropy (FA) in the posterior limbs of the internal capsules was determined

63 ial role for Gli2 in providing the remaining posterior limb patterning seen in Gli3 single mutants.

64 ing and why GLI2 can compensate for GLI3A in posterior limb patterning.

65 to be a key signal in establishing anterior-posterior limb polarity.

66 sitive cells, it is possible that cells with posterior limb skeletal fate also must be removed.

67 tion the Shh expression domain in the distal posterior limb, these factors cannot in themselves expla

68 depends upon continued Shh signaling in the posterior limb through mid-to-late bud stages.

69 n down-regulate hedgehog target genes in the posterior limb throughout the time Shh is expressed, ind

70 tribute to AP patterning specifically in the posterior limb, whereas GLIRs predominantly regulate ant

71 pread, involving the anterior limb, genu and posterior limb with the M3 projection located anteriorly