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System analysis identified distinct and common functional networks governed by transcription factor ASCL1, in glioma and small cell lung cancer.
Results indicate transcription factor Ascl1 protein functionalized with intracellular protein (show CKAP2 Proteins) delivery technology (Ascl1-IPTD) as a powerful tool for engineering neural tissue from pluripotent stem cells.
knocking down achaete-scute complex homologue-1 expression could significantly suppress the proliferation, migration, and invasion of laryngeal carcinoma cell in vitro and disorder epithelial-mesenchymal transformation-associated protein expression.
we found that CpG_6.7.8 of the achaete-scute homolog 1 CpG island is frequently hypermethylated in early-stage pulmonary neuroendocrine tumors, and this aberrant hypermethylation is negatively correlated with achaete-scute homolog 1 expression in this tumor spectrum
the first comprehensive high-resolution information on the structural propensities and conformational dynamics of Ascl1, is reported.
ASCL1 expression may determine the cell behaviors of SCLC partly through modifying EMT (show ITK Proteins) phenotypes.
This report identifies novel roles (show DDC Proteins)for the transcription factor Ascl1 in enteric gliogenesis and neurogenesis
ASCL1 expression is regulated by BRD4 (show BRD4 Proteins) is frequently overexpressed in small cell lung cancer.
Data show that chrysin suppressed cell proliferation and reducing expression of achaete-scute complex-like 1 (ASCL1) and the neuroendocrine biomarker chromogranin A (CgA (show CHGA Proteins)).
hASH1 is a specific marker to distinguish neuroendocrine tumors from squamous cell carcinomas and adenocarcinomas
we show that Ascl1 induces the transcription factor MyT1 (show MYT1 Proteins) while promoting neuronal differentiation...It promotes neuronal differentiation by counteracting the inhibitory activity of Notch (show NOTCH1 Proteins) signaling at multiple levels, targeting the Notch1 (show NOTCH1 Proteins) receptor and many of its downstream targets
ASCL1 and NEUROD1 distinguish heterogeneity in SCLC with distinct genomic landscapes.
Results are the first to define the timing of gliogenesis in the tuberal hypothalamus and indicate that Ascl1 is required to repress oligodendrocyte differentiation within this brain region.
This study showed that the combination of the microRNAs miR (show MLXIP Proteins)-124-9-9* with the transcription factor Ascl1 significantly increase neuronal reprogramming of Muller glia.
The chemical compound forskolin combined with Ascl1 induced approximately 80% of mouse fibroblasts to iPV neurons.
we observe that the early-born 5-HT (show DDC Proteins)(+) neurons are generated in Ascl1(-/-) mutants
the combination of gain- and loss-of-function experiments in the developing midbrain showed co-operative roles for Mgn (show HELT Proteins) and Mash1 genes in determining GABAergic identity.
This study findings demonstrate that Ascl1(CreERT2) and Glast (show SLC1A3 Proteins)(CreERT2) mouse lines enable simple and reliable labeling of adult-born GC lineages within restricted time windows.
results show that at least one of the differences between mammal and fish Muller glia that bears on their difference in regenerative potential is the proneural transcription factor Ascl1
This suggests that the maintenance of ASCL1 in its multiply phosphorylated state might prevent terminal differentiation in neuroblastoma (show ARHGEF16 Proteins).
These results establish maternal Asc1l as a key factor in establishing pre-patterning of the early embryo, acting in opposition to VegT and biasing the animal pole to adopt neural fates.
analysis of cell-cycle-dependent phosphorylation of the key reprogramming transcription factor Ascl1 on multiple serine-proline sites
This gene encodes a member of the basic helix-loop-helix (BHLH) family of transcription factors. The protein activates transcription by binding to the E box (5'-CANNTG-3'). Dimerization with other BHLH proteins is required for efficient DNA binding. This protein plays a role in the neuronal commitment and differentiation and in the generation of olfactory and autonomic neurons. Mutations in this gene may contribute to the congenital central hypoventilation syndrome (CCHS) phenotype in rare cases.
, achaete scute protein
, achaete-scute complex-like 1
, achaete-scute homolog 1
, class A basic helix-loop-helix protein 46
, achaete-scute complex homolog-like 1
, mammalian achaete scute homolog 1
, achaete-scute complex homolog 1 (Drosophila)
, achaete-scute complex homolog 1