Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human TWIST2 Antibodies:
anti-Mouse (Murine) TWIST2 Antibodies:
anti-Rat (Rattus) TWIST2 Antibodies:
Go to our pre-filtered search.
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 8 Pubmed References
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
Human Monoclonal TWIST2 Primary Antibody for WB - ABIN2734648
Ding, Tang, Fan, Wang, Wu, Xu, Xu, Gao, Wu: Overexpression of PEAK1 contributes to epithelial-mesenchymal transition and tumor metastasis in lung cancer through modulating ERK1/2 and JAK2 signaling. in Cell death & disease 2018
Together, these data suggest that the S18-2 protein induces epithelial to mesenchymal cell transition through the TWIST2/E-cadherin signalling and, consequently, CXCR4-mediated migration of prostate cancer cells.
TWIST2 induces miR-221-3p expression and consequently suppresses its direct target, THBS2, in lymphatic metastasis cervical cancer.
epithelial membrane protein 3 is a downstream effector of TWIST1/2 in inducing epithelial-to-mesenchymal transition in gastric cancer. Epithelial membrane protein 3 upregulation might be associated with gastric cancer metastasis and is a potential indicator of unfavorable overall survival and progression-free survival in gastric cancer patients
Findings indicated that HIF-2alpha promotes epithelial-mesenchymal transition in pancreatic cancer by regulating Twist2 binding to the promoter of E-cadherin.
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 and endowing the mesenchymal cell phenotype with Vimentin, which may be involved in the progression and prognosis of ovarian cancer.
MACC1 promotes vasculogenic mimicry in gastric cancer by regulating the HGF/c-Met-TWIST1/2 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 and to a lesser degree TWIST2 expressed within the tumor stroma could contribute to the epithelial-mesenchymal transition (EMT)-like tumor budding phenotype in colorectal cancers.
A substituted lysine at TWIST2 residue 75 results in Ablepharon Macrostomia Syndrome, whereas a glutamine or alanine yields Barber-Say Syndrome.
After chronic NOD2 stimulation, Twist1 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) and cervical squamous cell carcinoma.
Data have identified a novel TWIST2-p21 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.
TWIST1 and TWIST2 are expressed in skeletal muscle and remained unaltered in metabolic diseases.
Twist2 plays roles in osteogenesis differentiation, tumor formation and epithelial-mesenchymal transition.[review]
LPS promotes PDCD4 degradation via a pathway involving PI3K and mTOR, releasing Twist2, which induces IL-10 via c-Maf.
Twist2 is the key Twist isoform coupling aberrant signals from pithelial-mesenchymal transition (EMT) to senescence and is an important candidate biomarker for cervical cancer prognosis.
nuclear beta-catenin is accumulated in Twist2-induced EMT cells to facilitates ovarian cancer invasion and metastasis.
These data highlight a pivotal role for miR-138 in the regulation of colorectal cancer metastasis by targeting TWIST2.
Data indicate that the expression of Twist2 and Runx2 differs significantly in mesenchymal stromal cells from bone marrow (bmMSC) compared to MSC from term placenta (pMSC).
Tw2-tdTO(+) cells participate in lifelong maintenance of cardiac function, at least in part through de novo formation of CMs and fusion with preexisting CMs, as well as in the genesis of other cellular components of the adult heart.
Twist2 partially retains histone deacetylase 7 (HDAC7) in the nucleus and recruits it to the Nur77 promoter region to repress Nur77 in positively selected thymocytes.
Tw2 expression maintains progenitor cells in an undifferentiated state that is poised to initiate myogenesis in response to appropriate cues that extinguish Tw2 expression.
The Twist2-Cre, Osterix-Cre and osteocalcin-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 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 signaling/beta-catenin 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 mutations cause Saethre-Chotzen craniocynostosis suggests that they function independently in skin and bone development.
plays a critical role in inhibiting the differentiation of embryonic stem cells
Using the N-terminal domain of ADD1/SREBP1c as bait, we identified Twist2 (also known as Dermo-1), a basic helix-loop-helix (bHLH) protein, as a novel ADD1/SREBP1c interacting protein
Twist1 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, leading to IL-10 expression. It is essential for endotoxin tolerance.
copy number variant in the 5'-flanking region affects melanocyte development and pigmentation in belted cattle
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