ライフサイエンスコーパス: TWIST2

1 in FN-RMS tumors that express high levels of TWIST2.

2 even at known tumor suppressor genes such as TWIST2.

3 xpression by suppressing the Runx2 inhibitor Twist2.

4 inoma-1 cells by promoting the expression of Twist2.

5 Furthermore, Twist2, a transcriptional activator of c-Maf, is increas

6 We find that TWIST2 acts as a negative regulator of 3T3-L1 and primar

7 tified mutations fell in the basic domain of TWIST2 and altered the DNA-binding pattern of Flag-TWIST

8 are regulated by p53 and negatively regulate Twist2 and c-Maf expression in microglia and the RAW mac

9 Also, pro-EMT transcription factors TWIST1, TWIST2 and SNAIL showed an upregulation in SKOV3-MUC4 ce

10 Although human TWIST2 and TWIST1 encode highly homologous bHLH transcri

11 Humans have two paralogous genes, TWIST1 and TWIST2, and mutations in each gene have been identified

12 e mesenchymal markers (N-cadherin, Vimentin, Twist2, and ZEB1).

13 Twist1 and Twist2 are highly conserved members of the Twist subfami

14 Regulatory outcomes of Twist1 and Twist2 are themselves controlled by spatial-temporal exp

15 Gene expression studies nominated TWIST2 as a key effector downstream of BRAF.

16 We identify Twist2 as a previously unappreciated effector of adipocy

17 ible Twist2 expression system, we identified Twist2 as a reversible inhibitor of myogenic differentia

18 esophageal keratinocytes, we have identified Twist2 as an NFkB-responsive gene.

19 and a decrease in proliferation, implicating TWIST2 as an oncogene in RMS.

20 c chromatin and transcriptional landscape of Twist2 binding during myogenic differentiation.

21 n by stabilizing PDCD4 and thereby decreased Twist2 binding to the c-Maf promoter and induction of c-

22 TWIST2 blocks differentiation by inhibiting MYOD activit

23 During differentiation, Twist2 competes with MyoD at shared DNA motifs to direct

24 Moreover, Twist1 and Twist2 contributed to enhance expression and promoter bi

25 e, with chronic NOD2 stimulation, Twist1 and Twist2 contributed to the decreased expression and cytok

26 Mechanistically, TWIST2 controls H3K27 acetylation at distal enhancers by

27 e, after chronic NOD2 stimulation Twist1 and Twist2 coordinate the regulation of both transcriptional

28 In a subset of patients, methylation of TWIST2 correlated with mRNA expression.

29 A20 conditional knockout (KO) mice crossing Twist2-Cre and A20 floxed mice.

30 lung mesenchyme, we utilized the mesenchymal Twist2-Cre to drive expression of a constitutively activ

31 tly, complementing HDAC1 and HDAC3 in Twist1/Twist2-deficient monocyte-derived macrophages restored t

32 enetic silencing of the transcription factor TWIST2 (DERMO1) in Ig V(H) mutated CLL and describe a se

33 Although Twist1 and Twist2 did not coregulate each other's expression, they

34 Here, we show that knockdown of TWIST2 enables FN-RMS cells to exit the cell cycle and u

35 TWIST2 encodes a basic helix-loop-helix transcription fa

36 Comparison of wild-type and mutant TWIST2 expressed in zebrafish identified abnormal develo

37 with additional PRRs to increase Twist1 and Twist2 expression and Twist-dependent pathways.

38 ase chain reaction assays were used to study TWIST2 expression in CLL cells.

39 Through an inducible Twist2 expression system, we identified Twist2 as a reve

40 Consistently, Twist1 and Twist2 expression was increased after chronic NOD2 stimu

41 Meanwhile, Twist2 expression was not affected by the degree of hepa

42 examination of E-cadherin, Snail, Slug, and Twist2 expression was performed.

43 activity results in nearly complete loss of Twist2 expression, suggesting that this potential EMT-in

44 n of such processes requires that Twist1 and Twist2 function as molecular switches to activate and re

45 oduction of cre recombinase into the Dermo1 (Twist2) gene locus resulted in robust expression of CRE

46 osure in the intestinal environment, TWIST1, TWIST2, HDAC1, and HDAC3 were upregulated in human intes

47 Airway branching also appeared normal in Twist2-IKKbetaca embryos, with airway morphometry, elast

48 While Twist2-IKKbetaca lungs did not contain increased levels

49 While Twist2-IKKbetaca lungs had an increased number of macrop

50 Twist2-IKKbetaca lungs had increased staining for the va

51 differentiation appeared to be diminished in Twist2-IKKbetaca lungs.

52 Embryonic Twist2-IKKbetaca mice were generated in expected numbers

53 on may have been due to the inability of the Twist2-IKKbetaca transgene to induce inflammasome activi

54 The involvement of Twist1 and Twist2 in a broad spectrum of regulatory pathways highli

55 Expression of TWIST2 in a CLL cell line in which the promoter is methy

56 There exists a paucity of research on Twist2 in any cancer type; as such, these findings are i

57 , future studies should focus on the role of TWIST2 in CLL and related lymphoproliferative diseases.

58 ification events and increased expression of TWIST2 in fusion-negative RMS.

59 and altered the DNA-binding pattern of Flag-TWIST2 in HeLa cells.

60 lts indicate a regulatory role for PDCD4 and Twist2 in LPS-induced IL-10 production in macrophages.

61 e findings provide insights into the role of TWIST2 in maintaining an undifferentiated and tumorigeni

62 or the transcriptional repressors Twist1 and Twist2 in regulating PRR-induced cytokine outcomes is po

63 Knockdown of TWIST2 in RMS cells results in up-regulation of MYOGENIN

64 e identified a recurrent de novo mutation in TWIST2 in seven independent AMS-affected families, as we

65 Based on the known role of TWIST2 in silencing p53 function in other malignancies,

66 ilarities and differences between Twist1 and Twist2 in the context of myogenesis, osteogenesis, immun

67 (EMT) including E-cadherin, Snail, Slug, and Twist2, in the Egyptian population.

68 Although ectopic expression of AXL and TWIST2 individually in TAE684-sensitive parental cells l

69 TWIST2 is differentially methylated in CLL cells relativ

70 GFR overexpression and p120ctn inactivation, Twist2 is significantly upregulated.

71 TWIST2 knockdown also substantially reduces tumor growth

72 Previous phenotyping of Twist2 knockout mice and Setleis syndrome Twist2 (-/-) p

73 We confirm that Twist2 knockout mice have compromised lipid storage with

74 Notably, Setleis syndrome patients and Twist2 knockout mice have similar facial features, indic

75 Following identification and confirmation of TWIST2 methylation in CLL patients, we demonstrated that

76 of patient samples with mutated Ig V(H) show TWIST2 methylation, while only 16% of patient samples wi

77 ition sites in the 3' untranslated region of Twist2 mRNA that are predicted to interact with two p53-

78 driver genes, 17 of which, including TCF7L2, TWIST2, MSH2, DCC, EPHB1 and EPHB2 have been previously

79 Our results suggest that autosomal-dominant TWIST2 mutations cause AMS or BSS by inducing protean ef

80 pe IV FFDD patients and eight Type II or III TWIST2-negative FFDD patients revealed that three of the

81 Homozygous TWIST2 nonsense mutations, c.324C>T and c.486C>T, were i

82 sing CRISPR/Cas9 to genetically inactivate a TWIST2 orthologue, we suppressed the effects of BRAF(V60

83 s in the paralogous glutamic acid residue in TWIST2 (p.Glu75Ala, p.Glu75Gln and p.Glu75Lys).

84 of Twist2 knockout mice and Setleis syndrome Twist2 (-/-) patients noted deficiencies in subcutaneous

85 These data suggest that expression of TWIST2 plays a role in an early step of BRAF(V600E)-medi

86 r, we identify mechanisms wherein Twist1 and Twist2 promote chromatin modifications, resulting in mac

87 TWIST2 promoter methylation was identified by restrictio

88 RA was performed to study methylation of the TWIST2 promoter.

89 bHLH transcription factors, the finding that TWIST2 recessive mutations cause an FFDD and dominant TW

90 S and highlight the potential of suppressing TWIST2-regulated pathways to treat FN-RMS.

91 of the substituting amino acid: a lysine at TWIST2 residue 75 resulted in AMS, whereas a glutamine o

92 Additionally, Twist2 shapes the epigenetic landscape to drive chromati

93 and EndMT related gene (Snail, Slug, Twist1, Twist2, TGF-B) expression.

94 LPS disrupted the complex allowing Twist2 to bind to the c-Maf promoter.

95 The TWIST2 transcription factor is frequently overexpressed

96 cle progenitors, marked by expression of the Twist2 transcription factor, which fuses specifically to

97 e progenitor marked by the expression of the Twist2 transcription factor.

98 this region, the bHLH transcription factor, TWIST2, was initially sequenced on the basis of its know

99 We found that Twist1 and Twist2 were required for optimal cytokine downregulation

100 PDCD4 and the transcription factor Twist2 were shown to form a complex in untreated cells.

101 gulated the transcription factors Twist1 and Twist2, which bound to the promoters of the histone deac

102 a pathway involving PI3K and mTOR, releasing Twist2, which induces IL-10 via c-Maf.