Browse our anti-ASCL2 (ASCL2) Antibodies

Human Achaete-Scute Complex Homolog 2 (Drosophila) (ASCL2) interaction partners

1. this study shows that Ascl2 level was higher in peripheral blood mononuclear cells from Sjogren's syndrome patients compared with those from healthy controls

2. A novel HIF-1alpha (show HIF1A Antibodies)/Ascl2/miR (show MLXIP Antibodies)-200b regulatory feedback circuit in modulating EMT (show ITK Antibodies)-MET plasticity of CRC (show CALR Antibodies) cells, which could serve as a possible therapeutic target.

3. WiNTRLINC1 interacts with TCF4 (show TCF4 Antibodies)/beta-catenin (show CTNNB1 Antibodies) to mediate the juxtaposition of its promoter with the regulatory regions of ASCL2.

4. Ascl2 over-expression is associated with colorectal neoplasms.

5. expression of ASCL2 may identify an aggressive subgroup in lung squamous cell carcinoma

6. SEMA3F (show SEMA3F Antibodies) functions as a suppressor of colorectal cancer metastasis by down-regulating the ASCL2-CXCR4 (show CXCR4 Antibodies) signaling axis.

7. SNAIL1 (show SNAI1 Antibodies) combines competitive displacement of ASCL2 and epigenetic mechanisms to rapidly silence the EPHB3 (show EPHB3 Antibodies) tumor suppressor in colorectal cancer.

8. ASCL2 gene expression is regulated by miR (show MLXIP Antibodies)-200a/b/c, miR (show MLXIP Antibodies)-141 and miR429 levels in colon cancer.

9. Ascl2 directly initiates follicular T-helper cell development

10. These results suggest that ASCL2 might play an important role in gastric tumor growth and chemoresistance.

Cow (Bovine) Achaete-Scute Complex Homolog 2 (Drosophila) (ASCL2) interaction partners

1. More DNMT1 (show DNMT1 Antibodies) 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.

2. 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.

Mouse (Murine) Achaete-Scute Complex Homolog 2 (Drosophila) (ASCL2) interaction partners

1. Ascl2 inhibits myogenic differentiation by targeting MRFs and facilitates the generation of postnatal satellite cells.

2. 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.

3. The ascl2 forms a transcriptional switch that is both Wnt (show WNT2 Antibodies) responsive and Wnt (show WNT2 Antibodies) dependent to define stem cell identity.

4. Ascl2 directly initiates follicular T-helper cell development

5. TSSC3 (show PHLDA2 Antibodies) plays an important role in the differentiation from trophoblast stem cell to trophoblast progenitors and/or labyrinth trophoblasts through the TSSC3 (show PHLDA2 Antibodies)/PI3K/AKT (show AKT1 Antibodies)/MASH2 signaling pathway.

6. Elevated expression of Ascl2 in a Wnt (show WNT2 Antibodies) 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 (show APC Antibodies)(min) mouse.

7. Ascl2 knockdown results in tumor growth arrest by miRNA-302b-related inhibition of colon cancer progenitor cells

8. Partial loss of Ascl2 function affects all three layers of the mature placenta and causes intrauterine growth restriction.

9. Mash2 gene is preferentially expressed from the paternal allele.

10. The interval between Ins2 and Ascl2 is dispensable for imprinting centre function in the mouse model of Beckwith-Wiedemann Syndrome.

Pig (Porcine) Achaete-Scute Complex Homolog 2 (Drosophila) (ASCL2) interaction partners

1. 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.