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Human Polyclonal ASCL1 Primary Antibody for WB - ABIN1881074
Phi, Kim, Eun, Wang, Park, Choi, Kim, Park, Cho, Kim: Upregulation of SOX2, NOTCH1, and ID1 in supratentorial primitive neuroectodermal tumors: a distinct differentiation pattern from that of medulloblastomas. in Journal of neurosurgery. Pediatrics 2010
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Mouse (Murine) Monoclonal ASCL1 Primary Antibody for IHC, WB - ABIN2668587
Lo, Johnson, Wuenschell, Saito, Anderson: Mammalian achaete-scute homolog 1 is transiently expressed by spatially restricted subsets of early neuroepithelial and neural crest cells. in Genes & development 1991
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Human Polyclonal ASCL1 Primary Antibody for IHC (p), ELISA - ABIN542874
Chen, Biel, Borges, Thiagalingam, Nelkin, Baylin, Ball: Tissue-specific expression of human achaete-scute homologue-1 in neuroendocrine tumors: transcriptional regulation by dual inhibitory regions. in Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 1997
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Cow (Bovine) Polyclonal ASCL1 Primary Antibody for IHC, WB - ABIN2779585
Somasundaram, Reddy, Vinnakota, Britto, Subbarayan, Nambiar, Hebbar, Samuel, Shetty, Sreepathi, Santosh, Hegde, Hegde, Kondaiah, Rao: Upregulation of ASCL1 and inhibition of Notch signaling pathway characterize progressive astrocytoma. in Oncogene 2005
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Zebrafish (Danio rerio) Polyclonal ASCL1 Primary Antibody for ELISA - ABIN539735
Wullimann, Mueller: Expression of Zash-1a in the postembryonic zebrafish brain allows comparison to mouse Mash1 domains. in Brain research. Gene expression patterns 2003
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
a large subset of patient-derived glioblastoma stem cells (GSCs) express high levels of Achaete-scute homolog 1 (ASCL1), a proneural transcription factor involved in normal neurogenesis.
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 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 phenotypes.
This report identifies novel roles for the transcription factor Ascl1 in enteric gliogenesis and neurogenesis
ASCL1 expression is regulated by BRD4 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).
hASH1 is a specific marker to distinguish neuroendocrine tumors from squamous cell carcinomas and adenocarcinomas
marker for neurogenic potential in cultured retinal progenitor cells
Achaete-scute homolog 1 (ASCL1), a transcription factor required for proper development of pulmonary neuroendocrine cells, is essential for the survival of a majority of lung cancers with neuroendocrine features.
data suggest that a prominent down-regulation of hnRNP-A2/B1 during hypoxia is associated with the post-transcriptional suppression of hASH1 synthesis.
ASCL1 and RET expression defines a clinically relevant subgroup of lung adenocarcinoma characterized by neuroendocrine differentiation.
lentiviral overexpression of transcription factors ASCL1, SOX10, and NKX2.2 in NPCs was sufficient to induce Sox10 enhancer activity, OPC mRNA, and protein expression consistent with OPC fate
ASCL1 Promotes Wnt Signaling Directly by Repressing DKK1.
BRN2 is a higher level regulator than ASCL1 and ND1 and BRN2 might be involved in aggressiveness of small cell lung cancer.
Gene expression profiling revealed that permissive lines are typified by lower expression of the early neurogenic transcription factor ASCL1 and, conversely, by higher expression of the late neurogenic transcription factor NEUROD1.
Findings suggest that ASCL1 is a critical regulator of the proliferative capacity of gray and white matter NG2-glia in both the embryonic and adult spinal cord. These results highlight a role for ASCL1 in balancing oligodendrocyte precursor cells/NG2-glia proliferation and maintenance with myelin remodeling in the spinal cord throughout adult life.
Study results suggest that Mash1-positive cells could be differentiated to type III cells, not type II cells in the adult mouse taste buds.
Neurog2 and Ascl1 altered the expression of Ikaros and Foxg1.
we show that Ascl1 induces the transcription factor MyT1 while promoting neuronal differentiation...It promotes neuronal differentiation by counteracting the inhibitory activity of Notch signaling at multiple levels, targeting the Notch1 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-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(+) 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 and Mash1 genes in determining GABAergic identity.
This study findings demonstrate that Ascl1(CreERT2) and Glast(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.
CPAP regulates progenitor divisions and neuronal migration in the cerebral cortex downstream of Ascl1.
a single transcription factor, Ascl1, is sufficient to convert brain astrocytes into functional neurons
Mash1 is required for the expression of GAD67 and Dlx5 in taste bud cells.
the prethalamic factors Dlxs upregulated by Ascl1/Helt deficiency play unique roles in regulating thalamic progenitor specification.
GABAergic inducing activity of Ascl1 requires the direct transcriptional regulation of Ptf1a.
Ascl1 controls the number and distribution of astrocytes and oligodendrocytes in the gray matter and white matter of the spinal cord.
This study support a model whereby Ascl1 integrates inputs from both stimulatory and inhibitory signals and converts them into a transcriptional program activating adult neural stem cells.
dlx1a/2a act downstream of ascl1a but upstream of dlx5a/dlx6a and gad1b to activate GABAergic specification
bHLH transcription factor Ascl1a is essential for the specification of the intestinal secretory cells and mediates Notch signaling in the zebrafish intestine
Loss of ascl1a prevents secretory cell differentiation within the zebrafish intestinal epithelium resulting in a loss of distal intestinal motility
Data show that injury-dependent induction of Ascl1a suppressed expression of the Wnt signaling inhibitor, Dkk, and induced expression of the Wnt ligand, Wnt4a.
The Ascl1a regulates Muller glia dedifferentiation and retinal regeneration through a Lin-28-dependent, let-7 microRNA signalling pathway.
Expressed in the postsembryonic zebrafish brain
ash1a and ngn1 function in parallel redundant pathways to regulate neurogenesis downstream of flh
Ascl1a might act downstream of diencephalic fibroblast growth factor 3 (Fgf3) signaling to mediate some of the effects of Fgf3 on the developing adenohypophysis
Cellular correlates of proneural gene(ash1a) expression in the regenerating zebrafish retina.
ascl1a is essential for retina regeneration: within 4 h after retinal injury, ascl1a is induced in Muller glia.
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 homolog 1a
, pituitary absent
, pituitary-absent protein
, achaete-scute complex homolog 1