Human homeobox B2,HOXB2 ELISA Kit
- Known as:
- Human homeobox B2,HOXB2 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-0632
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human homeobox B2 HOXB2 ELISA Kit
Related genes to: Human homeobox B2,HOXB2 ELISA Kit
- 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: Human homeobox B2,HOXB2 ELISA Kit
Related articles to: Human homeobox B2,HOXB2 ELISA Kit
- Glioblastoma (GBM) is an aggressive primary brain tumor with unclear etiology. We aimed to identify causal risk genes by integrating single-cell RNA sequencing (scRNA-seq) and Mendelian randomization (MR). - Source: PubMed
Publication date: 2026/06/22
Huang ChongDong MinhaiYu YongjiaWang ChunxiHuang ChaojueLi TangSu XiangshengShi FengqiangFeng Daqin - The present study aimed to investigate the effects of microRNA (miR)‑5590‑3p on the biological functions of hepatocellular carcinoma (HCC) cells through the homeobox B2 (HOXB2)/MYC axis. The expression levels of miR‑5590‑3p, HOXB2 and MYC were measured in HCC tissues and cell lines, and the relationships between miR‑5590‑3p, HOXB2, and the clinicopathological characteristics and prognosis of patients with HCC were analyzed. The Cell Counting Kit‑8 assay assessed cell proliferation, flow cytometry measured apoptosis rate, and the Transwell and wound healing assays evaluated the invasive and migratory abilities of cells. The targeting interactions between miR‑5590‑3p and HOXB2, and between HOXB2 and MYC were assessed. In addition, a subcutaneous HCC xenograft model was established to assess the effects of miR‑5590‑3p on tumor growth. The results revealed that miR‑5590‑3p expression was downregulated in HCC tissues and cells, whereas HOXB2 and MYC expression were upregulated. Notably, low miR‑5590‑3p expression and high HOXB2 expression were both associated with a poor prognosis in patients with HCC. miR‑5590‑3p directly targeted and suppressed HOXB2, whereas HOXB2 promoted MYC transcription. Furthermore, downregulation of miR‑5590‑3p enhanced the invasion, migration and proliferation of Huh7 cells, and reduced their apoptotic rate. By contrast, miR‑5590‑3p overexpression or HOXB2 silencing decreased invasion, migration and proliferation, while increasing apoptosis. Moreover, HOXB2 overexpression reversed the inhibitory effect of miR‑5590‑3p upregulation on HCC cell proliferation. HOXB2 appeared to promote Huh7 cell proliferation and motility through MYC transcriptional activation, whereas miR‑5590‑3p overexpression suppressed tumor growth . In conclusion, miR‑5590‑3p may inhibit HCC cell proliferation and motility, and induce apoptosis by targeting HOXB2 and suppressing MYC transcription. - Source: PubMed
Publication date: 2026/05/08
Li BinZhou Lin - 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 the 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 in the menin-KMT2A target genes. We next assessed ziftomenib against 4 MEN1 (gene encoding menin) mutants (T349M, M327I, G331R, G331D) associated with clinical resistance to another menin inhibitor, revumenib. Ziftomenib retained antileukemic activity against T349M mutant cells and demonstrated low nanomolar potency (50% growth inhibition ≤ 25nM) against G331R cells, despite several-fold reduced potency relative to MEN1 wild-type cells, whereas the 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 the potent inhibitory activity toward these mutants. Ziftomenib has recently received US Food and Drug Administration 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
Miao HongzhiWu TaoPurohit TruptaChen DongKlossowski SzymonBorkin DmitryClegg BradleyRay JoshuaPark SeRaStevens RhiannonKim EunGiKempinska KatarzynaWang YiHe MiaoWen BoGoldman Joshua WAgrusa JenniferDing 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 - BACKGROUND: 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. METHODS: Public datasets and online platforms (PrognoScan, GEPIA2, TIMER, and Kaplan–Meier Plotter) were integrated to evaluate HOXB2 expression, survival outcomes, and correlations with tumor-infiltrating immune cell estimates in CRC and LGG. Associations between HOXB2 and immune marker genes were further assessed. In vitro, HOXB2 expression and biological effects were examined in glioma cells and normal brain cells using RT-qPCR, CCK-8 proliferation assays, Transwell invasion assays, and Western blotting. HOXB2 knockdown was additionally evaluated in the CRC cell line HT-29 using CCK-8, Transwell invasion assays, and Western blotting. RESULTS: Across three CRC cohorts (GSE17536, GSE17537, and GSE14333), higher HOXB2 expression was significantly associated with poorer overall survival (OS), disease-specific survival (DSS), and disease-free survival (DFS). In LGG, higher HOXB2 expression was associated with worse OS (HR = 1.8, P = 0.00084) and DFS (HR = 1.5, P = 0.014). TIMER analyses indicated that HOXB2 expression was positively correlated with estimated infiltration levels of B cells, CD4⁺ and CD8⁺ T cells, macrophages, neutrophils, and dendritic cells in colon adenocarcinoma (COAD), rectum adenocarcinoma (READ), and LGG, and was also correlated with marker genes related to tumor-associated macrophages, regulatory T cells, and exhausted T cells. In vitro, HOXB2 expression was higher in glioma cells than in normal brain cells; HOXB2 knockdown reduced glioma cell proliferation and invasion and was accompanied by a decreased p-P65/P65 ratio. In HT-29 cells, HOXB2 knockdown similarly suppressed proliferation and invasion, and Western blotting confirmed effective HOXB2 downregulation. CONCLUSIONS: Elevated HOXB2 expression is associated with adverse prognosis and with immune infiltration-related signatures in COAD, READ, and LGG. Together with in vitro findings, these results support HOXB2 as a potential prognostic biomarker and suggest a link between HOXB2 expression, immune-related features, and NF-κB-associated signaling; further pathway-focused and in vivo studies are needed to clarify underlying mechanisms and causality. - Source: PubMed
Publication date: 2026/02/13
Liu ZhenruiWen PuqiaoLiao YuxuanZhou DaweiWang HongyiXu RuofanZhang Zhen