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Mouse Anti-ASXL1 Recombinant Antibody (6E2) (CBMAB-A3824-YC)

Provided herein is a Mouse monoclonal antibody against Human Additional Sex Combs Like 1, Transcriptional Regulator. The antibody can be used for immunoassay techniques, such as ELISA, WB.
See all ASXL1 antibodies
Published Data
Mouse Anti-ASXL1 Recombinant Antibody (6E2) CBMAB-A3824-YC in WB
ASXL1 and ACTB protein levels were determined by Western blotting in transduced NB-4 cells. ...View More
Davies, C., Yip, B. H., Fernandez-Mercado, M., Woll, P. S., Agirre, X., Prosper, F., ... & Boultwood, J. (2013). Silencing of ASXL 1 impairs the granulomonocytic lineage potential of human CD 34+ progenitor cells. British journal of haematology, 160(6), 842-850.

Summary

Host Animal
Mouse
Specificity
Human
Clone
6E2
Antibody Isotype
IgG2a, κ
Application
ELISA, WB

Basic Information

Immunogen
ASXL1 (AAH64984.1, 1 a.a. ~ 84 a.a) full-length recombinant protein with GST tag.
Specificity
Human
Antibody Isotype
IgG2a, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

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

Format
Liquid
Buffer
PBS, pH 7.4
Preservative
None
Concentration
Batch dependent
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
additional sex combs like 1,transcriptional regulator
Introduction
ASXL1 is similar to the Drosophila additional sex combs gene, which encodes a chromatin-binding protein required for normal determination of segment identity in the developing embryo. ASXL1 is a member of the Polycomb group of proteins, which are necessar
Entrez Gene ID
171023
UniProt ID
Q8IXJ9
Alternative Names
Additional Sex Combs Like 1, Transcriptional Regulator; Additional Sex Combs Like Transcriptional Regulator 1; Additional Sex Combs Like 1 (Drosophila); Putative Polycomb Group Protein ASXL1; Additional Sex Combs-Like Protein 1; KIAA0978; BOPS; MDS;
Function
Probable Polycomb group (PcG) protein involved in transcriptional regulation mediated by ligand-bound nuclear hormone receptors, such as retinoic acid receptors (RARs) and peroxisome proliferator-activated receptor gamma (PPARG) (PubMed:16606617).
Acts as coactivator of RARA and RXRA through association with NCOA1 (PubMed:16606617).
Acts as corepressor for PPARG and suppresses its adipocyte differentiation-inducing activity (By similarity).
Non-catalytic component of the PR-DUB complex, a complex that specifically mediates deubiquitination of histone H2A monoubiquitinated at 'Lys-119' (H2AK119ub1) (PubMed:20436459).
Acts as a sensor of N6-methyladenosine methylation on DNA (m6A): recognizes and binds m6A DNA, leading to its ubiquitination and degradation by TRIP12, thereby inactivating the PR-DUB complex and regulating Polycomb silencing (PubMed:30982744).
Biological Process
Animal organ morphogenesis Source: GO_Central
Bone marrow development Source: Ensembl
Cell morphogenesis Source: Ensembl
Glomerular visceral epithelial cell development Source: Ensembl
Heart morphogenesis Source: Ensembl
Hemopoiesis Source: Ensembl
Homeostasis of number of cells Source: Ensembl
Lung saccule development Source: Ensembl
Monoubiquitinated histone H2A deubiquitination Source: UniProtKB
Negative regulation of fat cell differentiation Source: UniProtKB
Negative regulation of lipid storage Source: Ensembl
Negative regulation of peroxisome proliferator activated receptor signaling pathway Source: UniProtKB
Positive regulation of retinoic acid receptor signaling pathway Source: UniProtKB
Positive regulation of transcription by RNA polymerase II Source: UniProtKB
Protein deubiquitination Source: Reactome
Regulation of kidney size Source: Ensembl
Response to retinoic acid Source: UniProtKB
Thymus development Source: Ensembl
Transcription, DNA-templated Source: InterPro
Cellular Location
Nucleus
Involvement in disease
Bohring-Opitz syndrome (BOPS): A syndrome characterized by severe intrauterine growth retardation, poor feeding, profound mental retardation, trigonocephaly, prominent metopic suture, exophthalmos, nevus flammeus of the face, upslanting palpebral fissures, hirsutism, and flexion of the elbows and wrists with deviation of the wrists and metacarpophalangeal joints.
Myelodysplastic syndrome (MDS): A heterogeneous group of closely related clonal hematopoietic disorders. All are characterized by a hypercellular or hypocellular bone marrow with impaired morphology and maturation, dysplasia of the myeloid, megakaryocytic and/or erythroid lineages, and peripheral blood cytopenias resulting from ineffective blood cell production. Included diseases are: refractory anemia (RA), refractory anemia with ringed sideroblasts (RARS), refractory anemia with excess blasts (RAEB), refractory cytopenia with multilineage dysplasia and ringed sideroblasts (RCMD-RS); chronic myelomonocytic leukemia (CMML) is a myelodysplastic/myeloproliferative disease. MDS is considered a premalignant condition in a subgroup of patients that often progresses to acute myeloid leukemia (AML).
PTM
Ubiquitinated by TRIP12, leading to its subsequent degradation following binding N6-methyladenosine methylated DNA (m6A).

Xia, Y. K., Zeng, Y. R., Zhang, M. L., Liu, P., Liu, F., Zhang, H., ... & Ye, D. (2021). Tumor-derived neomorphic mutations in ASXL1 impairs the BAP1-ASXL1-FOXK1/K2 transcription network. Protein & cell, 12(7), 557-577.

Burgess, A. E., Kleffmann, T., & Mace, P. D. (2021). Oncogenic truncations of ASXL1 enhance a motif for BRD4 ET-domain binding. bioRxiv.

Hurtado, R., Guirales, F., & Tirado, C. A. (2021). ASXL1 Gene in AML. Journal of the Association of Genetic Technologists, 47(2).

Yamamoto, K., Goyama, S., Asada, S., Fujino, T., Yonezawa, T., Sato, N., ... & Kitamura, T. (2021). A histone modifier, ASXL1, interacts with NONO and is involved in paraspeckle formation in hematopoietic cells. Cell Reports, 36(8), 109576.

Bai, J., Chen, Z., Chen, C., Zhang, M., Zhang, Y., Song, J., ... & Zhou, Y. (2021). Reducing hyperactivated BAP1 attenuates mutant ASXL1-driven myeloid malignancies in human haematopoietic cells. Cancer Letters, 519, 78-90.

Kolovos, P., Nishimura, K., Sankar, A., Sidoli, S., Cloos, P. A., Helin, K., & Christensen, J. (2020). PR-DUB maintains the expression of critical genes through FOXK1/2-and ASXL1/2/3-dependent recruitment to chromatin and H2AK119ub1 deubiquitination. Genome research, 30(8), 1119-1130.

Asada, S., Fujino, T., Goyama, S., & Kitamura, T. (2019). The role of ASXL1 in hematopoiesis and myeloid malignancies. Cellular and Molecular Life Sciences, 76(13), 2511-2523.

Peng, H., Prokop, J., Karar, J., Park, K., Cao, L., Harbour, J. W., ... & Rauscher, F. J. (2018). Familial and somatic BAP1 mutations inactivate ASXL1/2-mediated allosteric regulation of BAP1 deubiquitinase by targeting multiple independent domains. Cancer research, 78(5), 1200-1213.

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

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