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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
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 (show WTIP Antibodies) and in the regulation of WT1 (show WT1 Antibodies) signaling during early kidney development
ASXL1 truncation mutations confer gain-of-function on the ASXL-BAP1 (show BAP1 Antibodies) 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 (show ASXL2 Antibodies) increases, the expression of adipogenic genes, most of which are PPARgamma (show PPARG Antibodies) targets
Asxl1 is needed for normal hematopoiesis.
Patients harbouring ASXL1 and/or CBL (show CBL Antibodies) 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 (show TET2 Antibodies), TET3 (show TET3 Antibodies), KDM1A (show KDM1A Antibodies) and MSH6 (show MSH6 Antibodies) were found in 25% of patients. TET2 (show TET2 Antibodies) or TET3 (show TET3 Antibodies), AKT1 (show AKT1 Antibodies) and RUNX1 (show RUNX1 Antibodies) were mutated in one patient each. ASXL1 was mutated within exon 12 in three cases
TET2 (show TET2 Antibodies), ASXL1, IDH1 (show IDH1 Antibodies), and IDH2 (show IDH2 Antibodies) Single Nucleotide Polymorphisms in Turkish Patients with Chronic Myeloproliferative Neoplasms.
Hypermethylation of the CTNNA1 (show CTNNA1 Antibodies) promoter was associated with unfavorable karyotype, and possessed the higher frequency of coexisting with ASXL1 and RUNX1 (show RUNX1 Antibodies) mutations.
Mutations in genes associated with epigenetic regulations such as DNMT3A (show DNMT3A Antibodies) and ASXL1 seem to play an important role in the pathogenesis of CML (show BCR Antibodies) progression and TKI-resistance independent of ABL1 (show ABL1 Antibodies) KD mutations
mutations in the SRSF2 (show SRSF2 Antibodies)/ASXL1/RUNX1 (show RUNX1 Antibodies) gene panel identified as significant prognostic markers in systemic mastocytosis
It was found that the absence of mutations in the SRSF2 (show SRSF2 Antibodies), 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.
ASXL1 mutation is associated with acute myeloid leukemia (show BCL11A Antibodies).
We examined all ASXL1 truncating variants in the ExAC database and determined most are likely somatic. Failure to consider somatic mosaicism may lead to the inaccurate assumption that conditions like BOS have reduced penetrance, or the misclassification of potentially pathogenic variants.
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