Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Mouse (Murine) ASXL1 Anticorps:
anti-Human ASXL1 Anticorps:
anti-Rat (Rattus) ASXL1 Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Human Polyclonal ASXL1 Primary Antibody pour IHC - ABIN965603
Fisher, Berger, Randazzo, Brock: A human homolog of Additional sex combs, ADDITIONAL SEX COMBS-LIKE 1, maps to chromosome 20q11. dans Gene 2003
Human Monoclonal ASXL1 Primary Antibody pour 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. dans British journal of haematology 2013
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.
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.
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.
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.
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