HMBOX1 siRNA_Lentivectors
- Known as:
- HMBOX1 siRNA_Lentivectors
- Catalog number:
- i009796d
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- HMBOX1 siRNA_Lentivectors
Related genes to: HMBOX1 siRNA_Lentivectors
- Gene:
- HMBOX1 NIH gene
- Name:
- homeobox containing 1
- Previous symbol:
- -
- Synonyms:
- HNF1LA, PBHNF, FLJ21616, HOT1
- Chromosome:
- 8p21.1-p12
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-24
- Date modifiied:
- 2018-02-13
Related products to: HMBOX1 siRNA_Lentivectors
Related articles to: HMBOX1 siRNA_Lentivectors
- To understand the mechanisms underlying the remarkable resistance of Göttingen minipigs to metabolic dysfunction-associated steatotic liver disease (MASLD), a multilevel transcriptomic analysis comparing their liver with those of humans, mice, and MASLD susceptible pig breeds was performed. This analysis revealed 692 genes uniquely differentially expressed in livers of Göttingen minipigs, linked to multiple metabolic and signaling pathways (e.g., AMPK signaling). Among these, 11 transcription factors (TFs), 3 hepatokines (DPP4, ITIH1, and ITIH3), and 6 additional secreted proteins (including PCSK9 and APOM) exhibited particularly strong differential expression and emerged as candidate mediators of MASLD resistance. This finding was further supported by weighted gene coexpression network analysis, which identified a core regulatory network driven by the TFs HMBOX1 and PATZ1, presumably regulating 41% of its differentially expressed genes. Collectively, these results suggest that a distinct transcriptional program involving HMBOX1/PATZ1 and their downstream targets, including secreted factors, contributes to the MASLD-resistant phenotype of Göttingen minipigs and may provide promising targets for the prevention and treatment of fatty liver disease. - Source: PubMed
Publication date: 2026/06/25
Gottmann PascalJonas WenkeRenner SimonePhilippou-Massier JuliaHommel TheresaDahlhoff MaikZeigerer AnjaWolf EckhardVogel HeikeSchürmann Annette - Hepatocellular carcinoma (HCC) represents the most common form of primary liver cancer and is characterized by a significant rate of recurrence. However, there is still a lack of effective therapeutic methods. Accumulating evidence has highlighted the importance of homeobox containing 1 (HMBOX1) in tumorigenesis. However, the relationship between HMBOX1 expression and HCC remains unclear. In the present study, through the analysis of public databases and staining analysis of tissue microarrays, it was found that compared with normal tissues, HMBOX1 was significantly downregulated in tumor tissues. Furthermore, through analyses such as Cell Counting Kit‑8 assay, wound healing assay and colony formation, it was found that overexpression of HMBOX1 could inhibit cell proliferation and migration, while silencing of HMBOX1 promoted tumor biological characteristics in HCC cell lines. The molecular biological mechanism was explored by using proteomics combined with bioinformatics analysis and western blotting. Mechanistically, AKT1 was identified as a downstream effector of HMBOX1, and protein tyrosine phosphatase non‑receptor type 1 (PTPN1) signaling might mediate the regulation of AKT1 by HMBOX1. tumor‑bearing experiments also verified the function of the HMBOX1/PTPN1/AKT1 pathway in HCC development. Taken together, the present findings revealed a new HMBOX1/PTPN1/AKT1 axis that inhibits tumor progression and provides new candidate therapy targets for HCC. - Source: PubMed
Publication date: 2026/01/23
Zhang ChenningJiang YuLiu JiahuiZhang WenyuQi JieWen QingZhao Hengli - Hepatocellular carcinoma (HCC) is one of the commonly lethal malignancies worldwide and represents a major global health-care challenge. We have previously demonstrated that plumbagin (PLB) could inhibit the development of tumor in liver, but the mechanism is still not fully clear. Here we identified a transcription repressor-homeobox containing 1 (HMBOX1) as a regulator in the development of HCC.Knockdown of HMBOX1 resulted into expansive of tumor cells, while overexpression led to growth inhibition. Mechanistically, PLB promoted HMBOX1 expression, leading to inactivation of PI3K/Akt-mTOR of liver cancer cells. Moreover, PLB also inhibited tumor formation in a xenograft transplantation model via PI3K/Akt/mTOR signaling. Collectively, our results suggested that HMBOX1 played a key role in PLB-induced inhibition of HCC growth through PI3K/Akt/mTOR signaling pathway. - Source: PubMed
Publication date: 2025/12/24
Wei YanfeiCheng TaoLiu HongMa YuanzhengLiu HuanDu YuanqinDeng Shuye - Acute myeloid leukemia (AML) is a molecularly and clinically heterogeneous disease. Nearly 50% of patients exhibit a normal karyotype, although genomic aberrations are recurrent. Translocations involving have increasingly been identified in patients with V617F-negative myeloproliferative neoplasms, as well as in various other hematologic diseases. Here, we present a unique case of a de novo AML patient with a t(8;9)(p22;p24) translocation, resulting in fusion. - Source: PubMed
Publication date: 2025/09/18
Catricalà SilviaDambruoso IreneBoni MarinaZappatore RitaPietra DanielaZappasodi PatriziaRossi MariannaBorsani OscarRumi ElisaArcaini Luca - Sepsis-induced myocardial dysfunction (SIMD) critically contributes to mortality in systemic inflammatory responses, driven by multifaceted mechanisms including dysregulated inflammation, immunosuppression, oxidative stress, and autonomic dysfunction. Emerging pathways involve m6A RNA methylation (mediated by methyltransferase METTL3), which coordinates inflammation, apoptosis, and ferroptosis through transcriptomic rewiring. Extracellular vesicles (EVs) serve dual roles: propagating injury via microRNA-885-5p/HMBOX1-induced pyroptosis and delivering therapeutic cargo (e.g., microRNA-223) to suppress inflammation. Mitochondrial dysfunction, marked by reactive oxygen species (ROS)-NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation and impaired sarco/endoplasmic reticulum calcium ATPase 2a (SERCA2a) stability, exacerbates metabolic disorder. Autonomic neuromodulation strategies, such as electroacupuncture and noninvasive vagus nerve stimulation, attenuate cardiac injury by rebalancing neuroimmune interactions. Complement hyperactivation (C5a-C5a receptor axis) and immune checkpoint inhibitors (e.g., anti-programmed death-ligand 1 [PD-L1] antibodies) show preclinical efficacy. However, challenges persist in addressing immune heterogeneity, dynamic biomarker profiling, and optimal therapeutic timing. This review bridges mechanistic discoveries to clinical innovation, proposing a paradigm shift toward precision therapies. Future research must bridge mechanistic insights with clinical innovation. By harmonizing pathophysiological understanding with precision medicine approaches, this synthesis underscores the potential to transform SIMD management from supportive care to targeted functional recovery. - Source: PubMed
Publication date: 2025/11/03
Liu CanLiu HanfengLi YunxingZeng YangxiWang XinyuMou YuhanLiao BinWan Juyi