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Mouse Anti-ASCL1 Recombinant Antibody (CBLNA-118) (CBMAB-1146-CN)

This product is a mouse antibody that recognizes ASCL1 of human. The antibody CBLNA-118 can be used for immunoassay techniques such as: WB, ELISA.
See all ASCL1 antibodies
Published Data

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat, Dog
Clone
CBLNA-118
Antibody Isotype
IgG1, κ
Application
WB, IP, IF, ELISA

Basic Information

Immunogen
Amino acids 181-236 mapping at the C-terminus of ASCL1 of human origin.
Specificity
Human, Mouse, Rat, Dog
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)1:50-1:500
ELISA1:100-1:1,000

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, 0.1% gelatin
Preservative
< 0.1% sodium azide
Concentration
0.2 mg/ml
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
Localized in aa.137-237

Target

Full Name
achaete-scute complex homolog 1 (Drosophila)
Introduction
Achaete-scute family bHLH transcription factor 1 (ASCL1) is a member of the basic helix-loop-helix (BHLH) family of transcription factors. ASCL1 activates transcription by binding to the E box (5'-CANNTG-3'). It plays a role in the neuronal commitment and differentiation and in the generation of olfactory and autonomic neurons. Mutations in ASCL1 gene may contribute to the congenital central hypoventilation syndrome (CCHS) phenotype in rare cases.
Entrez Gene ID
UniProt ID
Alternative Names
ASH1; HASH1; MASH1; bHLHa46
Function
Transcription factor that plays a key role in neuronal differentiation: acts as a pioneer transcription factor, accessing closed chromatin to allow other factors to bind and activate neural pathways. Directly binds the E box motif (5'-CANNTG-3') on promoters and promotes transcription of neuronal genes. The combination of three transcription factors, ASCL1, POU3F2/BRN2 and MYT1L, is sufficient to reprogram fibroblasts and other somatic cells into induced neuronal (iN) cells in vitro. Plays a role at early stages of development of specific neural lineages in most regions of the CNS, and of several lineages in the PNS. Essential for the generation of olfactory and autonomic neurons. Acts synergistically with FOXN4 to specify the identity of V2b neurons rather than V2a from bipotential p2 progenitors during spinal cord neurogenesis, probably through DLL4-NOTCH signaling activation. Involved in the regulation of neuroendocrine cell development in the glandular stomach (By similarity).
Biological Process
Adrenal chromaffin cell differentiation Source: Ensembl
Carotid body glomus cell differentiation Source: Ensembl
Cell maturation Source: Ensembl
Cellular response to magnetism Source: Ensembl
Central nervous system neuron development Source: Ensembl
Cerebral cortex development Source: Ensembl
Cerebral cortex GABAergic interneuron differentiation Source: UniProtKB
Commitment of neuronal cell to specific neuron type in forebrain Source: Ensembl
Heart development Source: Ensembl
Lung epithelial cell differentiation Source: UniProtKB
Lung neuroendocrine cell differentiation Source: Ensembl
Musculoskeletal movement, spinal reflex action Source: Ensembl
Negative regulation of apoptotic process Source: UniProtKB
Negative regulation of neuron differentiation Source: UniProtKB
Negative regulation of transcription, DNA-templated Source: UniProtKB
Negative regulation of transcription by RNA polymerase II Source: NTNU_SB
Neuroblast fate determination Source: Ensembl
Neuroblast proliferation Source: Ensembl
Neurogenesis Source: UniProtKB
Neuron development Source: UniProtKB
Neuron differentiation Source: UniProtKB
Neuron fate commitment Source: UniProtKB
Neuron fate specification Source: UniProtKB
Neuron migration Source: Ensembl
Noradrenergic neuron development Source: UniProtKB
Noradrenergic neuron fate commitment Source: UniProtKB
Notch signaling pathway Source: UniProtKB
Olfactory pit development Source: Ensembl
Oligodendrocyte development Source: Ensembl
Positive regulation of cell cycle Source: Ensembl
Positive regulation of neural precursor cell proliferation Source: Ensembl
Positive regulation of neurogenesis Source: Ensembl
Positive regulation of neuron apoptotic process Source: Ensembl
Positive regulation of neuron differentiation Source: UniProtKB
Positive regulation of Notch signaling pathway Source: Ensembl
Positive regulation of transcription by RNA polymerase II Source: UniProtKB
Regulation of epithelial cell differentiation Source: Ensembl
Regulation of gene expression Source: UniProtKB
Regulation of mitotic cell cycle Source: Ensembl
Regulation of neurogenesis Source: GO_Central
Regulation of timing of subpallium neuron differentiation Source: Ensembl
Regulation of transcription by RNA polymerase II Source: GO_Central
Response to epidermal growth factor Source: Ensembl
Response to folic acid Source: Ensembl
Response to lithium ion Source: Ensembl
Response to retinoic acid Source: UniProtKB
Sensory organ development Source: GO_Central
Spinal cord association neuron differentiation Source: Ensembl
Spinal cord oligodendrocyte cell fate specification Source: Ensembl
Stomach neuroendocrine cell differentiation Source: Ensembl
Subpallium neuron fate commitment Source: Ensembl
Sympathetic ganglion development Source: UniProtKB
Sympathetic nervous system development Source: UniProtKB
Ventral spinal cord interneuron fate commitment Source: UniProtKB
Vestibular nucleus development Source: Ensembl
Cellular Location
Nucleus

Nemoto, A., Kobayashi, R., Yoshimatsu, S., Sato, Y., Kondo, T., Yoo, A. S., ... & Okano, H. (2021). Direct Neuronal Reprogramming of Common Marmoset Fibroblasts by ASCL1, microRNA-9/9*, and microRNA-124 Overexpression. Cells, 10(1), 6.

Mamoor, S. (2020). ASCL1 is differentially expressed in the tumors of breast cancer patients treated with trastuzumab.

Enokido, T., Miyashita, N., Horie, M., Saito, A., & Nagase, T. (2020). ASCL1 suppress ZFP36L1 expression by regulating miR124-3p expression in lung adenocarcinoma.

Miyashita, N., Horie, M., Mikami, Y., Urushiyama, H., Fukuda, K., Makita, K., ... & Nagase, T. (2019). Effects of ASCL1 expression on tumorigenesis and immune cell infiltration in a syngenic mouse model of lung adenocarcinoma.

Amano, Y., Ando, T., Maemura, K., Sakatini, T., Sunohara, M., Watanabe, K., & Kage, H. (2018). Abstract B22: Exposure of AZD4547 FGFR-TKI to a lung squamous carcinoma cell line induces resistance by small cell lung cancer-like transformation associated with ASCL1.

Miyashita, N., Horie, M., Suzuki, H. I., Yoshihara, M., Djureinovic, D., Persson, J., ... & Nagase, T. (2018). An Integrative Analysis of Transcriptome and Epigenome Features of ASCL1–Positive Lung Adenocarcinomas. Journal of Thoracic Oncology, 13(11), 1676-1691.

Baronti, L., Hošek, T., Gil-Caballero, S., Raveh-Amit, H., Calçada, E. O., Ayala, I., ... & Brutscher, B. (2017). Fragment-Based NMR Study of the Conformational Dynamics in the bHLH Transcription Factor Ascl1. Biophysical journal, 112(7), 1366-1373.

Liu, Y. H., Tsai, J. W., Chen, J. L., Yang, W. S., Chang, P. C., Cheng, P. L., ... & Yu, J. Y. (2017). Ascl1 promotes tangential migration and confines migratory routes by induction of Ephb2 in the telencephalon. Scientific reports, 7(1), 1-17.

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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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