ライフサイエンスコーパス: TWIST2

1 even at known tumor suppressor genes such as TWIST2.

2 xpression by suppressing the Runx2 inhibitor Twist2.

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

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

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

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

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

8 Although human TWIST2 and TWIST1 encode highly homologous bHLH transcri

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

30 While Twist2-IKKbetaca lungs did not contain increased levels

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

32 Twist2-IKKbetaca lungs had increased staining for the va

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

34 Embryonic Twist2-IKKbetaca mice were generated in expected numbers

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

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

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

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

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

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

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

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

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

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

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

46 TWIST2 is differentially methylated in CLL cells relativ

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

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

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

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

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

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

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

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

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

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

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

58 TWIST2 promoter methylation was identified by restrictio

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

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

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

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

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

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

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

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