ライフサイエンスコーパス: cardiac muscle cell

1 te or inhibit contractility in demembranated cardiac muscle cells.

2 structural substates for SERCA expressed in cardiac muscle cells.

3 ) release through RyRs in neuronal cells and cardiac muscle cells.

4 lcNAcylation modulates DRP1 functionality in cardiac muscle cells.

5 sociation and underwent rapid endocytosis in cardiac muscle cells.

6 al differentiation of subtypes of neural and cardiac muscle cells.

7 on of contractile genes in smooth muscle and cardiac muscle cells.

8 helps to regulate the flow of Ca(2+) ions in cardiac muscle cells.

9 ss histological damage and less apoptosis of cardiac muscle cells.

10 in that regulates the flow of Ca(2+) ions in cardiac muscle cells.

11 -like growth factor 1 (IGF-1) stimulation in cardiac muscle cells.

12 cription factor is an important regulator of cardiac muscle cells.

13 owth factor-1 receptor (IGF-1R) signaling in cardiac muscle cells.

14 tly healthy young and aged mouse ventricular cardiac muscle cells.

15 to structural and functional alterations in cardiac muscle cells.

16 y, HGF was found to inhibit the apoptosis of cardiac muscle cells.

17 anscriptional regulatory effects of IGF-1 in cardiac muscle cells.

18 orm physical and functional connections with cardiac muscle cells.

19 not mediated through Bad phosphorylation in cardiac muscle cells.

20 phagic material and glycogen in skeletal and cardiac muscle cells.

21 tion confirmed the presence of CCRL1 mRNA in cardiac muscle cells.

22 Ca2+]i, regulate the contractile function of cardiac muscle cells.

23 is novel function of E1A is not exclusive to cardiac muscle cells.

24 factor messenger RNA expression in cultured cardiac muscle cells.

25 not sufficient, to trigger DNA synthesis in cardiac muscle cells.

26 l role in excitation-contraction coupling in cardiac muscle cells.

27 tain stabilized actin filament structures in cardiac muscle cells.

28 which are essential for enhancer function in cardiac muscle cells.

29 pathways do not regulate actin morphology in cardiac muscle cells.

30 tro differentiation of both rat skeletal and cardiac muscle cells.

31 er signals induce muscle fiber morphology in cardiac muscle cells.

32 se activity in the sarcoplasmic reticulum of cardiac muscle cells.

33 vity of the MCK enhancer in skeletal but not cardiac muscle cells.

34 uction of NOS2 by IL-1 beta and IFN gamma in cardiac muscle cells.

35 olarization along the length and deep within cardiac muscle cells.

36 in with a role in the repair of skeletal and cardiac muscle cells.

37 These results demonstrate that HGF protects cardiac muscle cells against apoptosis via a signaling p

38 ly, few methods can predict the state of the cardiac muscle cell and its metabolic conditions during

39 rowth factor I (IGF-I) inhibits apoptosis of cardiac muscle cells and improves myocardial function in

40 target of 5-HT(2A/2B) receptor signaling in cardiac muscle cells and suggest possible uses for 5-HT(

41 CS3 is a mechanical stress-inducible gene in cardiac muscle cells and that it directly modulates stre

42 ates, differentiation and diversification of cardiac muscle cells, and morphogenesis and patterning o

43 tribute to Purkinje neurons and skeletal and cardiac muscle cells, and participate in skin and heart

44 Spontaneous Ca(2)(+) waves in cardiac muscle cells are thought to arise from the seque

45 In cardiac muscle cells ArgBP2 is located in the Z-disks of

46 he inflammatory response and to the death of cardiac muscle cells by apoptosis.

47 at calmodulin (CaM) inhibits the activity of cardiac muscle cell Ca(2+) release channel ryanodine rec

48 the contractile strains produced by beating cardiac muscle cells can be optimized by substrate stiff

49 mRNA and protein increases during growth of cardiac muscle cells (cardiocytes) in vitro.

50 eton; their disruption within epithelial and cardiac muscle cells cause skin-blistering diseases and

51 Apoptosis of cardiac muscle cells contributes to the development of c

52 ed GATA-4 levels are functionally related to cardiac muscle cell death that can be induced by anthrac

53 enrichment > 2) were identified, including 'cardiac muscle cell differentiation'.

54 the protein level during skeletal as well as cardiac muscle cell differentiation.

55 helin-induced Purkinje fibers from embryonic cardiac muscle cells dramatically down-regulated cMyBP-C

56 about whether the epicardium is a source of cardiac muscle cells during heart development.

57 ss-inducible and NF-kappaB-dependent gene in cardiac muscle cells during the acute phase of hypertrop

58 been distinguished from those in contractile cardiac muscle cells; eg, 5' regulatory sequences of the

59 Cardiac muscle cells exhibit two related but distinct mo

60 Although mammalian cardiac muscle cells express bFGF, it is not known wheth

61 this function, we characterized apoptosis in cardiac muscle cells following serum deprivation.

62 s, an essential role for Sox17 was proven in cardiac muscle cell formation.

63 implicated in the regulation of hypertrophic cardiac muscle cell growth.

64 Cardiac muscle cells have an intrinsic ability to sense

65 e repair process, especially in skeletal and cardiac muscle cells, in which contraction-induced mecha

66 e cell types present in the heart, including cardiac muscle cells, indicating that the heart is not t

67 Hypertrophic growth of cardiac muscle cells is induced by a variety of physiolo

68 of dystroglycan matrix receptor function in cardiac muscle cells is likely important in the developm

69 lly results from a deficiency of specialized cardiac muscle cells known as cardiomyocytes, and a robu

70 ore, mutant mitochondrial 16S rRNA from aged cardiac muscle cells lacked this activity.

71 rced expression of POPDC1(S201F) in a murine cardiac muscle cell line (HL-1) increased hyperpolarizat

72 We have derived a cardiac muscle cell line, designated HL-1, from the AT-1

73 , we examined pro-ANP processing in a murine cardiac muscle cell line, HL-5.

74 gene, Nkx 2.5, and is an early marker of the cardiac muscle cell lineage.

75 Post-natal growth of cardiac muscle cells occurs by hypertrophy rather than d

76 logy mediated by direct viral destruction of cardiac muscle cells or by the virus-induced immune resp

77 Treatment of HL-1 cardiac muscle cells or isolated adult rat ventricular m

78 hanges in the constitutive properties of the cardiac muscle cell play a causative role in the develop

79 al, definitive endoderm/pancreatic and early cardiac muscle cells, respectively, in our CDM condition

80 In cardiac muscle cells, spontaneous store overload-induced

81 have recently demonstrated that a subset of cardiac muscle cells terminally differentiates as cells

82 al muscle MyBP-H is expressed in a subset of cardiac muscle cells that differentiate into Purkinje fi

83 s, terminally differentiate from a subset of cardiac muscle cells that respond to signals from endoca

84 (2A/2B) receptors and induces hypertrophy of cardiac muscle cells through a signaling pathway involvi

85 from the cell cycle precludes the ability of cardiac muscle cells to increase cell number after infar

86 enesis and temporally define the response of cardiac muscle cells to signals regulating chamber speci

87 Here we demonstrate that development of cardiac muscle cells was dramatically delayed and impair

88 IGF I actions on the apoptotic signaling of cardiac muscle cells, we have defined the effects of IGF

89 characteristics typical of embryonic atrial cardiac muscle cells were found consistently in the cult

90 sarcoplasmic reticulum (SR) in skeletal and cardiac muscle cells, where it is thought to bind to the