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Cow (Bovine) Polyclonal ASCL2 Primary Antibody für WB - ABIN2779425
Shahib, Martaadisoebrata, Kato: Detection of HASH2 (ASCL2) gene expression in gestational trophoblastic disease. in The Journal of reproductive medicine 2006
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Ascl2 negatively modulates pathogenic Th17cell differentiation via promoting IL-10 production, and alleviates intestinal inflammation.
R-spondin1/Wnt activated Ascl2 expression dose-dependently in the CD133(+)CD44(+) colorectal cancer population.
Study uncovers that SMYD3 controls Wnt induced activation of ASCL2 in cancer stem cells (CSCs) by regulating H3K4me3 status. These findings suggest that Wnt signals through a SMYD3-mediated epigenetic switch to promote ASCL2 expression and CSC maintenance in human gastric carcinoma (GC). Overexpression of SMYD3 and ASCL2 are associated with poor prognosis in GC patients.
High ASCL2 expression is associated with Drug Resistance in Colorectal Cancer.
SNP rs1335532 associated with multiple sclerosis is located in active CD58 enhancer region and creates a strong functional Ascl2-binding site.
ASCL2 increase by L1 overexpression enhanced its expression, cell motility, tumorigenesis and metastasis, similar to L1 overexpression. Its suppression in cells expressing L1 blocked these tumorigenic properties. In CRC tissue, ASCL2 was detected in the nuclei of cells at invasive areas of the tumor that also expressed L1. Results suggest that increased ASCL2 expression is a critical step in L1-mediated CRC progression.
ASCL2 was able to downregulate the expression level of miR223, contribute to Epithelial-Mesenchymal Transition and promote gastric tumor metastasis.
We address this paradox using basic helix-loop-helix (bHLH) transcription factors ASCL1, ASCL2, and MYOD1, crucial mediators of lineage specification..Although the ASCL factors and MYOD1 have some distinct DNA motif preference, it is not sufficient to explain the extent of the differential binding. All three factors can bind inaccessible chromatin and induce changes in chromatin accessibility and H3K27ac
this study shows that Ascl2 level was higher in peripheral blood mononuclear cells from Sjogren's syndrome patients compared with those from healthy controls
A novel HIF-1alpha/Ascl2/miR-200b regulatory feedback circuit in modulating EMT-MET plasticity of CRC cells, which could serve as a possible therapeutic target.
WiNTRLINC1 interacts with TCF4/beta-catenin to mediate the juxtaposition of its promoter with the regulatory regions of ASCL2.
Ascl2 over-expression is associated with colorectal neoplasms.
expression of ASCL2 may identify an aggressive subgroup in lung squamous cell carcinoma
SEMA3F functions as a suppressor of colorectal cancer metastasis by down-regulating the ASCL2-CXCR4 signaling axis.
SNAIL1 combines competitive displacement of ASCL2 and epigenetic mechanisms to rapidly silence the EPHB3 tumor suppressor in colorectal cancer.
ASCL2 gene expression is regulated by miR-200a/b/c, miR-141 and miR429 levels in colon cancer.
Ascl2 directly initiates follicular T-helper cell development
These results suggest that ASCL2 might play an important role in gastric tumor growth and chemoresistance.
Ascl2 knockdown results in tumor growth arrest by miRNA-302b-related inhibition of colon cancer progenitor cells
a stem cell specific transcription signature promoted by ASCL2 has been identified to be upregulated in a subset of liver metastases, those characterised by an 11p15.5 gain
More DNMT1 mRNA was detected in the transgenic somatic cell nuclear transfer (SCNT) group than the other three groups. Hsp 70.1 mRNA was detected in the in vitro fertilzation embryos. Mash2 mRNA was present at highest levels in transgenic SCNT embryos.
Mash2 is highly conserved across species and is specifically expressed in the bovine placenta. Bovine Mash2 appears to be maternally expressed after implantation, but the paternal genome plays a role in regulating expression.
ASCL2 is required for the emergence or early maintenance of glycogen trophoblast cells during development.
Ascl2 inhibits myogenic differentiation by targeting MRFs and facilitates the generation of postnatal satellite cells.
overexpression of the imprinted Ascl2 gene has considerable consequences for placental development, specifically for the parietal trophoblast giant cell and spongiotrophoblast lineages both of which express pregnancy-related hormones.
The ascl2 forms a transcriptional switch that is both Wnt responsive and Wnt dependent to define stem cell identity.
TSSC3 plays an important role in the differentiation from trophoblast stem cell to trophoblast progenitors and/or labyrinth trophoblasts through the TSSC3/PI3K/AKT/MASH2 signaling pathway.
Elevated expression of Ascl2 in a Wnt signalling dependent manner specifically in the stem cell compartment of the intestine neither increases tumour formation nor diminishes survival in a well established intestinal tumour model, the Apc(min) mouse.
Partial loss of Ascl2 function affects all three layers of the mature placenta and causes intrauterine growth restriction.
Mash2 gene is preferentially expressed from the paternal allele.
The interval between Ins2 and Ascl2 is dispensable for imprinting centre function in the mouse model of Beckwith-Wiedemann Syndrome.
Mash2 is a regulator of Krox24, Mob-1, and CXCR4 expression in cultured Schwann cells and negatively regulates their proliferation; a candidate for missing class B bHLH proteins in peripheral nerves
structure of the Mash2 gene and placental Mash2 expression at different gestational ages
ascl2 is a putative regulator of proliferation that is overexpressed in intestinal neoplasia
The combined results from these gain- and loss-of-function experiments imply that Ascl2 controls intestinal stem cell fate.
The lack of differential expression by microarray profiling of fetal tissues from swine parthenotes and control bi-parental fetuses supports lack of imprinting at ASCL2 in pigs.
This gene is a member of the basic helix-loop-helix (BHLH) family of transcription factors. It activates transcription by binding to the E box (5'-CANNTG-3'). Dimerization with other BHLH proteins is required for efficient DNA binding. Involved in the determination of the neuronal precursors in the peripheral nervous system and the central nervous system.
, achaete-scute complex-like 2
, achaete-scute homolog 2
, class A basic helix-loop-helix protein 45
, mammalian achaete/scute homologue 2
, transcription factor cash4
, achaete-scute complex homolog 2 (Drosophila)
, achaete-scute complex homolog-like 2
, achaete scute-like protein 2
, achaete-scute complex-like protein 2
, long transient receptor potential-related channel 5
, mammalian achaete scute homolog 2
, achaete-scute complex homolog 2