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anti-Mouse (Murine) ANKRD26 Antibodies:
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the methylation of specific CpGs at the Ankrd26 promoter occurs in mice during HFD treatment and causes the down-regulation of Ankrd26 expression, at least in part, by impairing p300 binding to its promoter. We propose that the epigenetic silencing of the Ankrd26 gene contributes to VAT inflammation following unhealthy dieting.
Deletion of the C-terminus of the protein encoded by Ankrd26 leads to changes in primary cilia in the brain, resulting in the disruption of the function of the melanocortin pathway and the HPA axis and leading to excessive food intake and obesity.
Data indicate that Ankrd26 is involved in regulation of food intake and in regulation of insulin/insulin receptor signaling in white adipose tissue; partial inactivation of Ankrd26 leads to obesity and, thus, to diabetes type 2.
conclude that Ankrd26 gene disruption promotes adipocyte differentiation at both the progenitor commitment and differentiation steps and that ERK activation plays a role in this process
obesity and gigantism may be caused by a disruption of the Ankrd26 gene
in a cohort of patients with suspected familial thrombocytopenia, the c.-140C>G mutation seems to be the most frequent ANKRD26 mutation.
Two cases with mutant ANKRD26 highlight that patients with thrombocytopenia 2 are at risk of being misdiagnosed with myelodysplastic syndrome and receiving undue myelosuppressive treatments. Because dysmegakaryopoiesis is a feature also of other forms of inherited thrombocytopenia, a genetic disorder must always be considered when a patient presents with isolated thrombocytopenia and dysmegakaryopoiesis.
investigation of one patient with the c.3G>A showed that mutation was associated with strong ANKRD26 overexpression in vivo, which is the proposed mechanism for predisposition to AML in THC2 patients
The findings of lifelong thrombocytopenia with mild/absent bleeding, family history of thrombocytopenia with normal platelet size and myeloid neoplasms should raise the suspicion of ANKRD26 mutated thrombocytopenia.
Molecular analysis identified a mutation located in the promoter of the ankyrin repeat domain 26 (ANKRD26) gene, c.-127A>T in normocytic thrombocytopenia.
thrombocytopenia with 5'UTR ANKRD26 gene mutation must be considered in case of a constitutional isolated thrombocytopenia, with a low bleeding tendency, associated with autosomal dominant transmission and normal platelet volume.
WASP, RUNX1, and ANKRD26 genes are important for normal TPO signaling and the network underlying thrombopoiesis.
The study supports the association of ANKRD26 mutations with thrombocytopenia 2 and a predisposition to myeloid malignancies.
ANKRD26 regulatory region mutations induce MAPK hyperactivation in familial thrombocytopenia
the missense mutations may paly a role in the pathogenesis of Autosomal-dominant nonsyndromic thrombocytopenia-2
Studies indicate that ANKRD26-RT is an insidious form of inherited thrombocytopenias that exposes patients to a low risk of bleeding but predisposes them to hematologic myeloid malignancies.
Ubiquitin/proteasome-rich particulate cytoplasmic structures are a characteristic feature of ANKRD26-related thrombocytopenia platelets and megakaryocytes.
The ANKRD26-related thrombocytopenia has to be taken into consideration in the differential diagnosis of isolated thrombocytopenias.
mutations in the 5' UTR of ANKRD26 are implicated in thrombocytopenia 2.
This gene encodes a protein containing N-terminal ankyrin repeats which function in protein-protein interactions. Mutations in this gene are associated with autosomal dominant thrombocytopenia-2. Pseudogenes of this gene are found on chromosome 7, 10, 13 and 16. Multiple transcript variants encoding different isoforms have been found for this gene.
, ankyrin repeat domain 26
, ankyrin repeat domain-containing protein 26