ライフサイエンスコーパス: telokin

1 affecting expression of the 220-kDa MLCK or telokin.

2 vs. WT ileum and was rescued by recombinant telokin.

3 mMLCK), as well as the non-catalytic product telokin.

4 and S19D to be not different from, wild-type telokin.

5 gnificantly different from that of wild-type telokin.

6 sphorylated MYPT1 levels by addition of S13D telokin.

7 c GMP (50 microM) phosphorylated recombinant telokin (10 microM) when added concurrently to ileum dep

8 Native telokin (5-20 microM), purified from turkey gizzard, and

9 The physiological importance of telokin, a 17-kDa smooth muscle-specific protein and tar

10 Incorporation of 32P into telokin, a smooth muscle-specific, 17-18-kDa, acidic (pI

11 A series of telokin and c-fos promoter chimeric and mutant reporter

12 Br-cGMP) induce phosphorylation of Ser-13 of telokin and relaxation of smooth muscle at constant calc

13 endogenous Elk-1, enhanced the expression of telokin and SM22alpha without affecting expression of sm

14 uscle cells increased the expression of only telokin and SM22alpha, suggesting that smooth muscle-spe

15 otein has a topology very similar to that of telokin and the titin Ig domains and thus it falls into

16 urrently to ileum depleted of its endogenous telokin, and their relaxant effects were mutually potent

17 e plasmon resonance studies showed that S13D telokin bound to full-length phospho-MYPT1.

18 nt myocardin induce expression of endogenous telokin but not c-fos in 10T1/2 fibroblast cells.

19 ting the normally approximately 5-fold lower telokin content in aorta vs. ileum smooth muscle.

20 he MLCK is bound directly to SMM through the telokin domain and some may also be bound to both SMM an

21 from turkey gizzard, and recombinant rabbit telokin, expressed in Escherichia coli and purified to >

22 ata suggest that GATA-6 selectively inhibits telokin expression by triggering the displacement of myo

23 r and stomach implicates HFH-1 in repressing telokin expression in epithelial cells.

24 that Hoxa10-1 is required for high levels of telokin expression in smooth muscle cells from uterus an

25 ing may explain the relatively low levels of telokin expression in the vascular system.

26 miR-1 repressed Telokin expression through direct targeting and by repre

27 ergistically with these proteins to regulate telokin expression.

28 cle-specific myosin heavy chain (SM MHC) and Telokin gene expression.

29 Transcription of the telokin gene is restricted to smooth muscle cells throug

30 In the present study, the mouse telokin gene was isolated, and a 370-bp (-190 to 180) mi

31 20 microM) also increased phosphorylation of telokin in intact ileum.

32 tion of endogenous phosphorylated MYPT1 with telokin in SM cells.

33 We conclude that telokin induces calcium desensitization in smooth muscle

34 Phospho-telokin is a target of elevated cyclic nucleotide concen

35 is suggests that cell-specific expression of telokin is likely mediated by both positive-acting facto

36 s in telokin KO smooth muscles indicate that telokin is not required for filament formation or stabil

37 lude that the mechanism of action of phospho-telokin is not through modulation of the MYPT1 phosphory

38 Results indicate that a primary role of telokin is to modulate force through increasing MLCP act

39 Kinase-related protein, also known as KRP or telokin, is an independently expressed protein product d

40 force by 8-Br-cGMP was attenuated by 50% in telokin KO intestinal smooth muscle.

41 t as a ligand and SM homogenates from WT and telokin KO mice as a source of endogenous proteins, we f

42 Normal thick filaments in telokin KO smooth muscles indicate that telokin is not r

43 8-Br-cGMP, was also significantly slowed in telokin KO vs. WT ileum and was rescued by recombinant t

44 Telokin null ileal smooth muscle homogenates compared to

45 uced Ca2+ desensitization, was determined in telokin null mice bred to a congenic background.

46 nhibited activity of phosphorylated MYPT1 in telokin-null ileum homogenates was restored to nonphosph

47 ic nucleotide-induced relaxation of force in telokin-null ileum muscle was reduced but not correlated

48 Here, we demonstrate that in telokin-null SM, both Ca(2+)-activated contraction and C

49 modulates the Ca2+ -desensitizing effect of telokin on force.

50 Conversely, a fragment of the telokin promoter (-94 to -49) increased the activity of

51 y, elements 5' and 3' of the CArG box in the telokin promoter act in concert with the CArG box to fac

52 myocardin by small interfering RNA decreased telokin promoter activity and expression in A10 SMCs.

53 2alpha gene fragment significantly increased telokin promoter activity in vascular smooth muscle cell

54 HFH-1 strongly represses telokin promoter activity when overexpressed in A10 vasc

55 HFH-1 inhibits telokin promoter activity, by binding to a forkhead cons

56 ysis revealed that GATA-6 strongly repressed telokin promoter activity.

57 binds to a nonconsensus binding site in the telokin promoter and Elk-1 binding is dependent on serum

58 irectly activated the smooth muscle-specific telokin promoter but did not activate the SM22alpha, smo

59 factors contribute to the activation of the telokin promoter in smooth muscle cells in a calcium-dep

60 n which the smooth muscle specificity of the telokin promoter is regulated by interactions between po

61 ate that an intact Elk-1 binding site in the telokin promoter is required for Elk-1 to maximally inhi

62 Mutational analysis of telokin promoter reporter genes demonstrated that the th

63 h muscle-restricted promoters, including the telokin promoter that does not contain a consensus Elk-1

64 ral smooth muscle-specific expression of the telokin promoter transgene is in marked contrast to the

65 ment (-288 to -116) was fused to the minimal telokin promoter was generated and characterized.

66 r binding to an adjacent CArG box within the telokin promoter, implying that HFH-1 must compete with

67 To identify proteins that bind to the telokin promoter, the AT-rich/CArG core of the promoter

68 t to repress the myocardin activation of the telokin promoter, this repression is not as complete as

69 Our results show that the SMC-specific telokin promoter, which contains only a single CArG box,

70 EF significantly increased the activity of a telokin promoter-reporter gene; this activation was furt

71 Hoxb8 bind directly to multiple sites in the telokin promoter.

72 y, Foxf1 directly binds to and activates the telokin promoter.

73 nsensus site adjacent to the CArG box in the telokin promoter.

74 blocked myocardin-induced activation of the telokin promoter.

75 to an AT-rich region within the core of the telokin promoter.

76 site located within an AT-rich region of the telokin promoter.

77 A novel approach with chimeric SM22alpha/telokin promoters was used to identify gene regulatory m

78 tentiated through phosphorylation by cGMP in telokin-rich smooth tissues.

79 alanine (A; non-phosphorylatable) mutants of telokin showed that the S13D mutant was more effective t

80 er hand, Hoxb8 inhibited the activity of the telokin, SM22alpha, and smooth muscle alpha-actin promot

81 smooth muscle-restricted proteins, including telokin, SM22alpha, and smooth muscle alpha-actin.

82 contractile and regulatory proteins such as telokin, smooth muscle gamma-actin, and Cav1.2b in visce

83 ound that only in the presence of endogenous telokin, thiophospho-GST-MYPT1 co-precipitated with phos

84 MP- and/or cAMP-dependent phosphorylation of telokin up-regulates its relaxant effect.

85 Endogenous telokin was lost from ileum during prolonged permeabiliz

86 estricted inhibitor of MLC2 phosphorylation, Telokin, was ectopically expressed in the myocardium, al

87 Recombinant and native gizzard telokins were phosphorylated, in vitro, by the catalytic

88 us had the same relaxant effect as wild-type telokin, whereas the C-terminal peptide (residues 142-15

89 lectively inhibited expression of endogenous telokin, while simultaneously increasing expression of o

90 vectors, increased expression of endogenous telokin without altering expression of myosin light chai

91 agonized by the addition of recombinant S13D telokin, without changing the inhibitory phosphorylation

92 e in the Ca2+ force relationship occurred in telokin WT and knockout (KO) aortas, presumably reflecti