Browse our anti-ASCL2 (ASCL2) Antibodies

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

1. ASCL2 was able to downregulate the expression level of miR223, contribute to Epithelial-Mesenchymal Transition and promote gastric tumor metastasis.

2. 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

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

4. 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.

5. WiNTRLINC1 interacts with TCF4/beta-catenin to mediate the juxtaposition of its promoter with the regulatory regions of ASCL2.

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

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

8. SEMA3F functions as a suppressor of colorectal cancer metastasis by down-regulating the ASCL2-CXCR4 signaling axis.

9. SNAIL1 combines competitive displacement of ASCL2 and epigenetic mechanisms to rapidly silence the EPHB3 tumor suppressor in colorectal cancer.

10. ASCL2 gene expression is regulated by miR-200a/b/c, miR-141 and miR429 levels in colon cancer.

11. Ascl2 directly initiates follicular T-helper cell development

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

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

14. 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

15. These findings suggest that increased protein levels and DNA binding of USF1 and USF2 mediate the inhibitory effects of hypoxia and of Mash-2 on CYP19 gene expression in human placenta

16. These results suggest that PACE4 expression is down-regulated by Hash-2/Mash-2 in both human and rat placenta and that many bioactive proteins might be regulated by PACE4 activity.

17. ascl2 is a putative regulator of proliferation that is overexpressed in intestinal neoplasia

18. Negative expression of HASH2 in complete hydatidiform moles (CM) but positive expression in malignant tumors suggests the presence of a specific mechanism for inactivation of the HASH2 gene in CM and reactivation in invasive moles or choriocarcinoma

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

1. 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.

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 is required for the emergence or early maintenance of glycogen trophoblast cells during development.

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

3. 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.

4. The ascl2 forms a transcriptional switch that is both Wnt responsive and Wnt dependent to define stem cell identity.

5. Ascl2 directly initiates follicular T-helper cell development

6. 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.

7. 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.

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

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

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

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

12. 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

13. structure of the Mash2 gene and placental Mash2 expression at different gestational ages

14. ascl2 is a putative regulator of proliferation that is overexpressed in intestinal neoplasia

15. The combined results from these gain- and loss-of-function experiments imply that Ascl2 controls intestinal stem cell fate.

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.