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Basic helix-loop-helix (bHLH) transcription factors have been implicated in cell lineage determination and differentiation. Additionally we are shipping TWIST2 Proteins (6) and many more products for this protein.
Showing 10 out of 73 products:
Human Monoclonal TWIST2 Primary Antibody for IHC (p), ELISA - ABIN566756
Murakami, Ohkuma, Nakamura: Molecular mechanism of transforming growth factor-beta-mediated inhibition of growth arrest and differentiation in a myoblast cell line. in Development, growth & differentiation 2008
Show all 7 references for ABIN566756
Human Polyclonal TWIST2 Primary Antibody for WB - ABIN871769
Lee, Lowe, Flanagan, Kuchler, Glackin: Human Dermo-1 has attributes similar to twist in early bone development. in Bone 2000
Human Polyclonal TWIST2 Primary Antibody for IF, WB - ABIN530431
Wade, Brinas, Welfare, Wicking, Farlie: Twist2 contributes to termination of limb bud outgrowth and patterning through direct regulation of Grem1. in Developmental biology 2012
Findings indicated that HIF-2alpha (show EPAS1 Antibodies) promotes epithelial-mesenchymal transition in pancreatic cancer by regulating Twist2 binding to the promoter of E-cadherin (show CDH1 Antibodies).
A homozygous missense mutation in the TWIST2 gene was described in 3 siblings affected by Setleis syndrome. An alteration of bHLH domain, and loss of transcription factor's function was predicted due to protein substitution.
TWIST2 regulates epithelial-mesenchymal transition by depriving the epithelial cell phenotype of E-cadherin (show CDH1 Antibodies) and endowing the mesenchymal cell phenotype with Vimentin (show VIM Antibodies), which may be involved in the progression and prognosis of ovarian cancer.
MACC1 (show MACC1 Antibodies) promotes vasculogenic mimicry in gastric cancer by regulating the HGF/c-Met-TWIST1 (show TWIST1 Antibodies)/2 signaling pathway.
In patients with no duplication/triplication of the 1p36.22p36.21 region and no mutations in TWIST2, there are mutation(s) in one of the 30 genes in this region or mutations in other as yet unidentified genes at different locations
Data suggest that TWIST1 (show TWIST1 Antibodies) and to a lesser degree TWIST2 expressed within the tumor stroma could contribute to the epithelial-mesenchymal transition (EMT (show ITK Antibodies))-like tumor budding phenotype in colorectal cancers.
A substituted lysine at TWIST2 residue 75 results in Ablepharon Macrostomia Syndrome, whereas a glutamine (show GFPT1 Antibodies) or alanine yields Barber-Say Syndrome.
After chronic NOD2 (show NOD2 Antibodies) stimulation, Twist1 (show TWIST1 Antibodies) and Twist2 coordinate the regulation of both transcriptional activators and repressors, thereby mediating optimal cytokine down-regulation.
Results show that Twist2 expression was gradually increased during the progression from normal cervical squamous epithelium to cervical intraepithelial neoplasia (CIN (show PDXP Antibodies)) and cervical squamous cell carcinoma.
Data have identified a novel TWIST2-p21 (show CDKN1A Antibodies) axis that regulates the cell cycle of both normal and leukemic hematopoietic cells, which implicates TWIST2 as a novel tumor suppressor in human acute myeloid leukemia (show BCL11A Antibodies).
The Twist2-Cre, Osterix (show SP7 Antibodies)-Cre and osteocalcin (show BGLAP Antibodies)-Cre lines to generate conditional beta1 integrin deletions, were used to investigate the role of beta1 integrins on skeletal phenotype.
Twist-2 was involved in endotoxin tolerance through inhibiting NF-kappaB (show NFKB1 Antibodies) transactivation and cytokines transcriptional activities.
Twist2 functions as a tumor suppressor in osteosarcoma cells.
we identify Twist2 as a key regulator of survival, invasion and anchorage-independent growth in the aneuploid cells
Wnt (show WNT2 Antibodies) signaling/beta-catenin (show CTNNB1 Antibodies) is absolutely required and sufficient for Dermo1 expression and dermal cell identity in the cranium.
Twist2 is required for normal corneal keratocyte proliferation and eyelid morphogenesis in the mouse.
TWIST2 recessive mutations cause an focal facial dermal dysplasias and dominant TWIST1 (show TWIST1 Antibodies) mutations cause Saethre-Chotzen craniocynostosis suggests that they function independently in skin and bone development.
Using the N-terminal domain of ADD1/SREBP1c (show SREBF1 Antibodies) as bait, we identified Twist2 (also known as Dermo-1), a basic helix-loop-helix (bHLH) protein, as a novel ADD1/SREBP1c (show SREBF1 Antibodies) interacting protein
Twist1 (show TWIST1 Antibodies) and Twist2 factors are cross-regulated and inhibit bone specific gene expression and other helix-loop-helix proteins
Twist-2 activates the transcription factor c-Maf (show MAF Antibodies), leading to IL-10 (show IL10 Antibodies) expression. It is essential for endotoxin tolerance.
Basic helix-loop-helix (bHLH) transcription factors have been implicated in cell lineage determination and differentiation. The protein encoded by this gene is a bHLH transcription factor and shares similarity with another bHLH transcription factor, Twist. It is thought that during osteoblast development this protein may inhibit osteoblast maturation and maintain cells in a preosteoblast phenotype. Two transcript variants encoding the same protein have been found for this gene.
twist homolog 2 (Drosophila)
, twist-related protein 2
, class A basic helix-loop-helix protein 39
, dermis-expressed protein 1
, twist homolog 2
, twist-related bHLH protein Dermo1
, dermis expressed 1
, dermo-1 protein