HOXB2 antibody - N-terminal region (ARP35647_P050)
- Known as:
- HOXB2 (anti-) - N-terminal region (ARP35647_P050)
- Catalog number:
- arp35647_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HOXB2 antibody - N-terminal region (ARP35647_P050)
Related genes to: HOXB2 antibody - N-terminal region (ARP35647_P050)
- Gene:
- HOXB2 NIH gene
- Name:
- homeobox B2
- Previous symbol:
- HOX2, HOX2H
- Synonyms:
- -
- Chromosome:
- 17q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-08-25
Related products to: HOXB2 antibody - N-terminal region (ARP35647_P050)
Related articles to: HOXB2 antibody - N-terminal region (ARP35647_P050)
- The protein-protein interaction between menin and KMT2A (histone lysine methyltransferase 2A) plays a critical role in acute leukemia with KMT2A rearrangements, nucleophosmin 1 (NPM1) mutations and nucleoporin 98 rearrangements, and represents an emerging opportunity for therapeutic intervention. Here, we report development and comprehensive evaluation of the activity of ziftomenib as an orally bioavailable, highly potent and selective small molecule inhibitor of the menin-KMT2A interaction. In leukemia cells and primary patient samples with the menin-KMT2A dependency, ziftomenib profoundly inhibited proliferation, reduced clonogenic potential and induced differentiation, which was associated with strong downregulation of the menin-KMT2A target genes, including MEIS1, HOXA9 and HOXB2. In xenografts and patient-derived xenograft models of KMT2A-rearranged leukemia, ziftomenib induced leukemia regression or reduced leukemia burden, accompanied by a pronounced reduction of the menin-KMT2A target genes. We next assessed ziftomenib against four MEN1 (gene encoding menin) mutants (T349M, M327I, G331R, G331D) associated with clinical resistance to another menin inhibitor revumenib. Ziftomenib retained anti-leukemic activity against T349M mutant cells and demonstrated low-nanomolar potency (GI50≤25 nM) against G331R cells, despite several-fold reduced potency relative to MEN1 wild-type cells, whereas M327I and G331D mutants were resistant. The crystal structures of ziftomenib in complex with menin wild-type, T349M or G331R mutants revealed a similar binding mode of ziftomenib to these menin variants, rationalizing potent inhibitory activity towards these mutants. Ziftomenib has recently received FDA approval for adult patients with NPM1-mutated acute myeloid leukemia and continues to be evaluated clinically in leukemias with NPM1 or KMT2A alterations, both as monotherapy and in combinations. - Source: PubMed
Publication date: 2026/03/18
Miao HongzhiWu TaoPurohit TruptaChen DongKlossowski SzymonBorkin DmitryClegg BradleyRay Joshua MartinPark SeRaStevens RhiannonKim EunGiKempinska KatarzynaWang YiHe MiaoWen BoGoldman Joshua WAgrusa Jennifer EDing ChaoSulis Maria LuisaSun DuxinMody RajenKim Annette SRen PingdaLi Lian-ShengLiu YiBurrows FrancisKessler LindaCierpicki TomaszGrembecka Jolanta - The pathogenesis of sarcopenia involves complex molecular mechanisms, and treatment remains challenging, with a lack of reliable diagnostic biomarkers. The objective of this study is to identify biomarkers that may be linked to sarcopenia, examine how these biomarkers correlate with immune cell infiltration, and investigate the genes that exhibit a causal relationship with sarcopenia. - Source: PubMed
Publication date: 2026/02/26
Wu YaoqiCai XiaoqingFan ShiwenZhao LinaJiao YingyingChen TongkaiLiu MantingSong Yafang - HOXB2 is a homeobox transcription factor whose dysregulation has been reported in multiple malignancies; however, its clinical relevance and associations with the tumor microenvironment (TME) in colorectal cancer (CRC) and low-grade glioma (LGG) remain incompletely characterized. - Source: PubMed
Publication date: 2026/02/13
Liu ZhenruiWen PuqiaoLiao YuxuanZhou DaweiWang HongyiXu RuofanZhang Zhen - To investigate the effect of SHP2 on the STAT3/TET3/HOXB2 signaling pathway in osteosarcoma, and its role in the proliferation, migration and invasion of osteosarcoma cells. First, bioinformatics analysis was used to identify relevant expressed genes. In vitro experiments, the expression levels of SHP2, p-STAT3, TET3, HOXB2, c-Myc, NANOG, NUSAP1 proteins in 143B cells and MG63 cells were detected by Western blot assay. The levels of TET3 and HOXB2 were detected by immunofluorescence double staining. Cell proliferation was detected by plate clone formation and CCK-8 assay. Cell migration was detected by scratch assay, and cell migration and invasion were detected by Transwell assay. Overexpression of SHP2 promotes osteosarcoma proliferation by upregulating STAT3, TET3 and HOXB2 proteins. VEGF activates RTK receptors and induces SHP2 autophosphorylation, which in turn activates STAT3 and enhances TET3 synthesis. TET3 then promotes HOXB2 transcription through demethylation. HOXB2 further upregulate the expression of c-Myc, NANOG and NUSAP1, ultimately driving the proliferation, migration and invasion of osteosarcoma and promoting tumor progression. This study confirmed that SHP2 promotes the proliferation, invasion and invasive ability of osteosarcoma cells by activating the STAT3/TET3/HOXB2 pathway, providing a new strategy for targeted treatment of osteosarcoma. - Source: PubMed
Publication date: 2026/01/24
Yang HuaJi Jiangfeng - Lung adenocarcinoma (LUAD) is the fifth leading cause of cancer-related deaths worldwide. Due to nonspecific early symptoms, most patients with LUAD are diagnosed at advanced stages, marked by extensive metastases and a poor 5-year survival rate. Although HOXC6 has been implicated in promoting LUAD tumorigenesis, its upstream and downstream mechanisms remain largely unknown. This study aimed to elucidate the role and molecular mechanisms of HOXC6 in LUAD progression. RT-qPCR, IHC, western blot, and IF staining assays were used to assess the expression levels of genes and proteins. Proliferation, migration, and invasion were evaluated using the CCK-8, scratch, and Transwell assays, respectively. ChIP, RIP, and dual-luciferase assays were performed to explore the interactions among HOXC6, HOXB2, circRAPGEF5, and HNRNPC. Additionally, in vivo xenograft and metastatic mouse models were established. FISH was used to detect circRAPGEF5 expression in LUAD tissues. circRAPGEF5 knockdown inhibited LUAD cell proliferation, migration, and invasion as well as tumor growth and metastasis in vivo. Mechanistically, circRAPGEF5 enhanced the stability of HOXC6 mRNA by interacting with HNRNPC, thereby promoting HOXC6 expression. HOXC6 transcriptionally activated HOXB2. Notably, HOXC6 overexpression counteracted the inhibitory effects of circRAPGEF5 knockdown on LUAD progression. Collectively, our findings indicated that circRAPGEF5 facilitates LUAD progression and metastasis by stabilizing HOXC6 mRNA via HNRNPC and promoting HOXB2 transcription. These results suggest that targeting circRAPGEF5 and HOXC6 can be a promising approach for LUAD treatment. - Source: PubMed
Jia LiZhang LijuanWang DongjieWang MengyaoZhang XinZhang Wei