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anti-Mouse (Murine) ASXL1 Antibodies:
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Human Monoclonal ASXL1 Primary Antibody for ELISA, WB - ABIN949894
Davies, Yip, Fernandez-Mercado, Woll, Agirre, Prosper, Jacobsen, Wainscoat, Pellagatti, Boultwood: Silencing of ASXL1 impairs the granulomonocytic lineage potential of human CD34? progenitor cells. in British journal of haematology 2013
Human Polyclonal ASXL1 Primary Antibody for IHC - ABIN965603
Fisher, Berger, Randazzo, Brock: A human homolog of Additional sex combs, ADDITIONAL SEX COMBS-LIKE 1, maps to chromosome 20q11. in Gene 2003
Mutant ASXL1 cooperates with BAP1 to promote myeloid leukemogenesis.
study underscores the ASXL1-cohesin interaction as a novel means to maintain normal sister chromatid separation and regulate gene expression in hematopoietic cells.
This study proposed the first Asxl1 mutation knock-in mouse model and showed mutated Asxl1 lowered the threshold of MN1-driven engraftment and exhibited distinct biological functions on physiological and malignant hematopoiesis, although it was insufficient to lead to blood malignancies.
Loss of Asxl1 alters self-renewal and cell fate of bone marrow stromal cell, leading to Bohring-Opitz-like syndrome in mice.
implicate Asxl1 in the maintenance of podocyte structure via its association with Wtip and in the regulation of WT1 signaling during early kidney development
ASXL1 truncation mutations confer gain-of-function on the ASXL-BAP1 complex.
Asxl1-/- fetuses have reduced body weight and display cleft palate, anophthalmia as well as ventricular septal defects and a failure in lung maturation.
Asxl1 functions as a tumor suppressor to maintain hematopoietic cell homeostasis
C-terminal-truncating Asxl1 mutations inhibited myeloid differentiation and induced myelodysplastic syndrome-like disease
Constitutive loss of Asxl1 results in developmental abnormalities, including anophthalmia, microcephaly, cleft palate, and mandibular malformations. Hematopoietic-specific deletion results in cytopenia and dysplasia with increased hematopoietic stem cells
ASXL1 represses, whereas ASXL2 increases, the expression of adipogenic genes, most of which are PPARgamma targets
Asxl1 is needed for normal hematopoiesis.
Asxl1and Asxl2 are expressed as multiple transcripts, at varying levels, in adult tissues and in embryonic stem cells analyzed by Northern blot, and exhibit similar expression patterns suggesting they may be co-regulated
ASXL1 is a novel coactivator of RAR that cooperates with SRC-1
Asxl1 function is determined by its interacting partners or chromatin environment to bring about changes in gene regulation.
Identification of driver and subclonal mutations in ASXL1 and IDH1/IDH2 genes in an Argentine series of patients with myelofibrosis.
very particular "pre-CMML"-MDS cases seem to be well characterized by enhanced genetic instability, justifying multiple co-mutations, and by the constant feature of early ASXL1 mutation.
There were no significant differences between the clinical and laboratory characteristics of ASXL1-mutated (ASXL1) chronic myelomonocytic leukemia and ASXL1-nonmutated (ASXL1) chronic myelomonocytic leukemia patients.
Data indicate that additional Sex Comb-Like 1 protein (ASXL1)-mut were associated with poor prognosis in de novo AML with trisomy 8 as the sole aberration.
our data further validate the prognostic role of ASXL1 mutations in chronic myelomonocytic leukemia
The authors demonstrate that BAP1 deubiquitinase activity and its association with ASXL1 to form the Polycomb repressive deubiquitinase complex (PR-DUB) impacts TRAIL sensitivity implicating transcriptional modulation as an underlying mechanism.
Prognostic interaction between bone marrow morphology and SF3B1 and ASXL1 mutations in myelodysplastic syndromes with ring sideroblasts
EZH2 mutations in chronic myelomonocytic leukemia cluster with ASXL1 mutations and their co-occurrence is prognostically detrimental.
Transcriptome analysis revealed that ASXL1 mutations altered differentiation of U937 cells by disturbing genes involved in myeloid differentiation.
This study identifies the unique role of JAG1-induced Notch activation in the pathogenesis of multiple myeloma. This is of significant clinical relevance due to the prevalence of truncating ASXL1 mutations and their effect on clinical outcome in patients with myeloid malignancies
Evidence of a key role for ASXL1 in erythropoiesis, ASXL1 loss hinders erythroid development/maturation.
Patients harbouring ASXL1 and/or CBL mutations (n = 8, 8 deaths, median OS = 11 months) had a significantly worse OS as compared to those without either mutation (n = 11, 4 deaths, median OS = 84 months) (P = 0.0002) (Fig 1a).
Patients with mutations 6 showed higher rate of achieving major molecular response than those<6 (P=0.0381). Mutations in epigenetic regulator, ASXL1, TET2, TET3, KDM1A and MSH6 were found in 25% of patients. TET2 or TET3, AKT1 and RUNX1 were mutated in one patient each. ASXL1 was mutated within exon 12 in three cases
TET2, ASXL1, IDH1, and IDH2 Single Nucleotide Polymorphisms in Turkish Patients with Chronic Myeloproliferative Neoplasms.
Hypermethylation of the CTNNA1 promoter was associated with unfavorable karyotype, and possessed the higher frequency of coexisting with ASXL1 and RUNX1 mutations.
Mutations in genes associated with epigenetic regulations such as DNMT3A and ASXL1 seem to play an important role in the pathogenesis of CML progression and TKI-resistance independent of ABL1 KD mutations
mutations in the SRSF2/ASXL1/RUNX1 gene panel identified as significant prognostic markers in systemic mastocytosis
It was found that the absence of mutations in the SRSF2, ASXL1, and/or RUNX1gene panel at baseline and a reduction of the KIT D816V allele burden more than 25% at month 6 are the most favorable predictors for improved survival in midostaurin-treated advanced systemic mastocytosis patients.
Mutation in ASXL1 gene is associated with chronic myelomonocytic leukemia.
This gene 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. The protein is a member of the Polycomb group of proteins, which are necessary for the maintenance of stable repression of homeotic and other loci. The protein is thought to disrupt chromatin in localized areas, enhancing transcription of certain genes while repressing the transcription of other genes. The protein encoded by this gene functions as a ligand-dependent co-activator for retinoic acid receptor in cooperation with nuclear receptor coactivator 1. Mutations in this gene are associated with myelodysplastic syndromes and chronic myelomonocytic leukemia. Alternative splicing results in multiple transcript variants.
additional sex combs like 1
, additional sex combs-like protein 1
, putative Polycomb group protein ASXL1