Ask about this productRelated genes to: HOXA9 antibody
- Gene:
- HOXA9 NIH gene
- Name:
- homeobox A9
- Previous symbol:
- HOX1G, HOX1
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2014-11-18
Related products to: HOXA9 antibody
Related articles to: HOXA9 antibody
- The HOXA gene locus coordinates body patterning, hematopoiesis, and differentiation. While studying blood phenotype-associated variation within the HOXA locus, we identified a genetic variant, rs17437411, associated with globally reduced blood counts, protection from blood cancers, and variation in anthropometric phenotypes. We found that this variant disrupts the activity of a previously unstudied antisense long non-coding RNA (lncRNA) located between HOXA7 and HOXA9, which we named HOXA opposite-strand transcript, stem-cell regulator, antisense mid-cluster between loci (HOTSCRAMBL). The HOTSCRAMBL variant disrupts lncRNA function and reduces human hematopoietic stem cell (HSC) self-renewal. Mechanistically, HOTSCRAMBL enables appropriate expression and splicing of HOXA genes in HSCs, most notably HOXA9, in an SRSF2-dependent manner. Given the critical role of HOXA gene expression in some blood cancers, we also demonstrate that HOTSCRAMBL variation or deletion compromises HOXA-dependent acute myeloid leukemias. Collectively, we show how insights from human genetic variation can uncover critical regulatory processes required for effective developmental gene expression. - Source: PubMed
Publication date: 2026/05/01
Lyu PengAgarwal GauravGuo Chun-JieSychla AdamBourgeois WallaceYe TianyiWeng ChenAntoszewski MateuszJoubran SamanthaCaulier AlexisPoeschla MichaelArmstrong Scott ARouskin SilviSankaran Vijay G - Chronic myeloid leukemia (CML) is a hematologic malignancy originating from hematopoietic stem cells with the fusion oncogene BCR-ABL1 on the Philadelphia chromosome, which drives the abnormal proliferation of leukemic blast cells within the bone marrow microenvironment. While previous research has primarily focused on the hematopoietic compartment, the functional contribution of the bone marrow microenvironment to the CML pathology remains understudied. We investigated the changes in the peripheral nervous system in the bone marrow with myeloid leukemia via immunofluorescence staining of tyrosine hydroxylase (TH) and calcitonin gene-related peptide (CGRP) antibodies in mouse with NUP98-HOXA9- and BCR-ABL1-expressing myeloid leukemia. We found that the TH-positive fibers were significantly reduced, while no overt changes were observed in CGRP-positive nerves in the bone marrow. The reduction in TH-positive nerve cells was also evident in the spleen. Human patient gene expression data suggested that the levels of sympathetic nerve receptor expression change during the blastic transformation of human CML. Our findings indicate that the sympathetic nervous system regulates the pathogenesis of myeloid leukemia and could play a crucial role in the disease progression of myeloid leukemia. - Source: PubMed
Publication date: 2026/04/13
Okigawa SayumiInafuku HibikiHattori AyunaIto Takahiro - - Source: PubMed
- Menin scaffolds the oncogenic histone-lysine-N-methyltransferase (KMT2A)-fusion protein (FP) complex in r and wild-type complex in -m acute myeloid leukemia (AML). Menin inhibitors (MIs) are effective in -r AML and -m AML. However, not all patients respond to MIs as monotherapy. In this preclinical study, we demonstrate that the MI ziftomenib, in combination with the XPO1 inhibitor selinexor, synergistically inhibited the growth of multiple r and -m AML cell lines (CI<1). The combination suppressed colony formation in primary CD34+ r progenitor cells without affecting normal stem cells. Robust apoptosis and decreased G2/M populations were also evident. The combination downregulated HOXA9 and MEIS1 while upregulating monocytic differentiation marker CD11b in both the AML molecular signatures. RNA sequencing and proteomic analysis in r revealed suppression of multiple bona fide menin-KMT2A target genes. Our mechanistic studies also identified a novel role of XPO1 in stabilizing menin's binding to chromatin and its interactions with KMT2A and KMT2A/MLLT3. XPO1 inhibitor-mediated disruption of these interactions, particularly in combination with ziftomenib, synergistically impairs oncogenic transcriptional programs. , combination therapy improved survival in both MV4;11 and OCI-AML3 cell line and primary patient-derived - and -m AML xenograft models in NSG mice, effective even at reduced drug doses. These preclinical findings demonstrate that simultaneous inhibition of the menin-KMT2A interaction and XPO1 can be a more effective translational strategy for treating r and -m AML than MI monotherapy to deepen responses and delay/prevent relapses. - Source: PubMed
Publication date: 2026/03/13
Uddin Md HafizDhiman SandhyaHan YufenAboukameel AmroDhillon VikramAguillar JeffBuck StevenDeol AbhinavBoerner Julie LPolin LisaKessler LindaBurrows FrancisYang JayAzmi Asfar SMaciejewski Jaroslaw PCutler JevonDu YangBalasubramanian Suresh Kumar - Gene regulation through translation is critical for spatiotemporal protein expression. Internal ribosomal entry sites (IRESes) mediate mRNA-specific translation by recruiting ribosomes to 5' untranslated regions. Circular RNAs (circRNAs), naturally occurring and stable RNA species, are increasingly used as synthetic tools for sustained therapeutic protein translation by IRES-driven initiation. However, the functionality of different IRESes in synthetic circRNAs remains sparsely characterized. We systematically examine circRNA reporter translation by viral and cellular IRESes in human cells and in diverse translation systems. Improved circRNA purification by urea-PAGE and RNase R-treatment removes contaminants that induce RNA sensing. Viral CVB3 and HCV, as well as cellular , , and IRESes, effectively drive circRNA translation. We also establish circRNA translation in an improved human cell-free extract that recapitulates IRES-dependent regulation, and allows for precise engineering of HCV IRES-mediated translation. These findings inform IRES selection for synthetic circRNA translation relevant for circRNA-based medicines. - Source: PubMed
Publication date: 2026/03/29
Koch PhilippArendrup Frederic S WLim ChaeheeNarayanan SamyuktaAdam AminaClamer MassimilianoLund Anders HChen Chun-KanLeppek Kathrin