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anti-Mouse (Murine) ASXL1 Antibodies:
anti-Human ASXL1 Antibodies:
anti-Rat (Rattus) 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
Asxl1 played a critical role in regulating genes associated with neural differentiation without affecting self-renewal of mouse embryonic stem cells.
Concomitant mutations of ASXL1 and RAS pathway genes were associated with aggressive progression of myeloid malignancies
the osteoclastogenesis of ASXL1 deficiency does not involve classical RANKL- or M-CSF-stimulated molecules such as MAPKs and c-Fos but activation of NFATC1 by reversal of suppressive histone methylation.
These findings reveal that ASXL1 mutations confer hematopoietic stem cells with an altered epigenome and increase susceptibility for leukemic transformation.
ASXL1 mutation is associated with hematological disorders caused by derepression of p16Ink4a through aberrant PRC1-mediated histone modification.
ASXL1 truncation is associated with myeloid malignancy.
ASXL1(aa1-587) plays a gain-of-function role in promoting myeloid malignancies.
Asxl1 deficiency leads to growth retardation.
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.
Studied ASXL1 mutations in myeloid neoplasms, and their association with survival and clinical outcomes in patients with myeloid neoplasms.
ASXL1 mutations identified MDS patients predicted to show inferior response to treatment with both hypomethylating agents and lenalidomide.
study of ASXL1 gene alterations in myelodysplastic syndrome patients with isolated 20q deletion
PV patients with co-mutations of ASXL1 and JAK2V617F had a poor MF-free survival.
Screening for ASXL1 and SRSF2 mutations is imperative for treatment decision-making in otherwise low or intermediate-1 risk patients with myelofibrosis.
MDS associated with myeloproliferative features had more EZH2, ASXL1 and STAG2 mutations
Study found that in patient with acute myeloid leukemia (AML) ASXL1 mutations were associated with older age, secondary AML and higher peripheral leukocytosis. More frequently co-occurrence of ASXL1 mutations observed with trisomy 8 and chromosome 11 aberrations but a negative correlation was found with myelodysplastic syndromes-related cytogenetic abnormalities.
EZH2 and ASXL1 mutations are associated with defective erythropoiesis in Primary myelofibrosis.
ASXL1 c.1934dup variant is associated with myeloid malignancy.
People with ASXL1rs3746609 A/G genotype were related to lower prevalence of myelodysplastic syndromes (MDS). This SNPs was associated with certain laboratory features in MDS patients
our findings show a high frequency of ASXL1 mutations in children and young adults with CML.
a novel ASXL1-OGT axis and raise the possibility that this axis has a tumor-suppressor role in myeloid malignancies.
ASXL1 mutational status significantly and independently predicts poor outcomes in patients with myelodysplastic syndromes (MDS) with multilineage dysplasia
Mutations in the ASXL1 gene are associated with poor prognosis in patients with myelofibrosis.
Study confirmed that ASXL1 c.1934dupG is a somatic mutation that is usually clonally related and associated with somatic mutations in TET2, EZH2, IDH2, RUNX1, NRAS and DNMT3A. The pattern of clonal evolution suggests that this particular mutation might be an early mutational event occurring in the principal clonal population and can serve as a clonal marker for persistent/relapsing disease.
data demonstrate that ASXL1-compromised cells benefit from loss of TP53 but do not lead to malignant transformation.
differentially methylated CpG sites in ASXL1 mutated Myelofibrosis cases are found in regulatory regions that could be associated with aberrant gene expression of ASXL1 target genes.
CSF3R T618I, ASXL1 G942 fs and STAT5B N642H trimutation co-contribute to a rare chronic neutrophilic leukaemia manifested by rapidly progressive leucocytosis, severe infections, persistent fever and deep venous thrombosis.
Loss of ASXL1 expression is associated with tumorigenesis.
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