Ask about this productRelated genes to: HMOX2 Blocking Peptide
- Gene:
- HMOX2 NIH gene
- Name:
- heme oxygenase 2
- Previous symbol:
- -
- Synonyms:
- HO-2
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-15
- Date modifiied:
- 2017-12-15
Related products to: HMOX2 Blocking Peptide
Related articles to: HMOX2 Blocking Peptide
- Ischemic heart failure (IHF) is a major cause of cardiovascular morbidity worldwide, characterized by complex tissue remodeling and inflammation. However, reliable molecular biomarkers for early diagnosis and a systematic understanding of the associated immune-stromal microenvironment remain limited. Identifying specific transcriptomic signatures may enhance diagnostic precision and reveal novel therapeutic targets. - Source: PubMed
Publication date: 2026/03/31
Sun YangChang YuFeng YezhiSong BinghuiZhou Yanan - Nanovesicles (NVs)-generated directly from donor cells-have emerged as important mediators of intercellular communication, drug delivery devices, and in therapeutic applications, including regenerative biology. Top-down strategies to enhance the potential regenerative efficacy of NVs following cell hypoxic stress are poorly understood. Here, NVs were generated using rapid extrusion directly from human induced pluripotent stem cells (iPSC) under basal and hypoxic-associated conditions, identifying select pluripotent/stem cell maintenance markers associated with NV composition. We performed adaptive cellular remodeling of iPSC to hypoxic preconditioning over 2, 4, and 6 h, demonstrating that NV form and composition are context-dependent on hypoxia and its duration. Hypoxic exposure modifies the NV temporal protein landscape of networks involved in wound healing (FLNA, MYH9, ACTC1), hypoxia response (HMOX2, HMOX1, PGK), extracellular matrix remodeling (ITGA6, MFGE8, ITGB1), and tissue repair (HSP A5/A8/H1/20/27/70/90, GJA1, HMGB1, ILK). Importantly, we highlight that the NV proteome is dependent and highly consistent on temporal exposure of donor cells to hypoxia, indicating a platform to regulate NV phenotype, tailored toward their potency. Here, we show NVs exhibit a distinct proteome landscape associated with regulation in reactive oxygen species generation and cell/tissue survival (enhanced 2-4 h hypoxia), wound healing and angiogenesis (enhanced 4-6 h hypoxia), and tissue repair, hypoxic response, and metabolic/energy production (enhanced 6 h hypoxia). Extended hypoxic cell exposure (at 4-6 h) regulates NV function in a hypoxic time-dependent manner, with NVs significantly promoting tubule formation of endothelial cells in hypoxic conditions (p < 0.0001). Here, we detailed the capacity of hypoxic cell conditioning to mediate NV phenotype and function in a temporal manner as a platform to enhance functional and potential regenerative therapeutic efficacy of NVs. - Source: PubMed
Publication date: 2026/04/05
Lozano JonathanRai AlinPhang Ren JCross JonathonLim Shiang YGreening David W - Sirtuin 3 (SIRT3), a mitochondrial NAD-dependent deacetylase, plays a central role in regulating mitochondrial metabolism, oxidative stress, and cell survival. Although SIRT3 has been implicated in angiogenesis, apoptosis, and inflammation, its global proteomic impact on the brain remains unclear. This study aimed to systematically characterize alterations in angiogenesis-, apoptosis-, chemokine-, and cytokine-related proteins in the brains of SIRT3 knockout (SIRT3 KO aka SIRT3/) mice compared with wild-type (WT) controls. - Source: PubMed
Publication date: 2026/02/28
He QingpingKhan SamiaWang LinlinIbeanu Gordon CLi P Andy - Despite the importance of the gut microbiome to health, the role of human genetic variation in shaping its composition remains poorly understood. Here we report genome-wide association analyses of harmonized metagenomic data from 16,017 adults in four Swedish population-based studies, with replication in 12,652 people from the Norwegian HUNT study. We identified variants in the OR51E1-OR51E2 locus, encoding sensors for microbiome-derived fatty acids, associated with microbial richness. We further identified 15 study-wide significant genetic associations (P < 5.4 × 10) involving eight loci and 14 common bacterial species, of which 11 associations at six loci were replicated. The results confirm previously reported associations at LCT, ABO and FUT2, and provide evidence for new loci MUC12, CORO7-HMOX2, SLC5A11, FOXP1 and FUT3-FUT6, with supporting data from metabolomics and gene expression analyses. Our findings link gut microbial variation genetically to gastrointestinal functions, including enteroendocrine fatty acid sensing, bile composition and mucosal layer composition. - Source: PubMed
Publication date: 2026/02/13
Dekkers Koen FPertiwi KamalitaBaldanzi GabrielLundmark PerHammar UlfMoksnes Marta RiiseCoward EivindNethander MariaSalih Ghassan AliMiari MariamNguyen DiemSayols-Baixeras SergiEklund Aron CHolm Jacob BakNielsen H BjørnVolpiano Camila GazollaMéric GuillaumeThangam ManonanthiniHakaste LiisaTuomi TiinamaijaAhlqvist EmmaSmith Christopher AAllen MarieReimann FrankGribble Fiona MOhlsson ClaesHveem KristianMelander OlleNilsson Peter MEngström GunnarSmith J GustavMichaëlsson KarlÄrnlöv JohanOrho-Melander MarjuFall Tove - Accurate detection of therapy-resistant cancer cell populations remains a major barrier to diagnostic precision and improved patient outcomes. Tumor-initiating cells (TICs), which drive recurrence and metastasis, are difficult to visualize because multidrug resistance transporters limit intracellular probe retention. This study investigated the molecular determinants of TiNIR, a near-infrared probe that targets TICs by binding heme oxygenase 2 (HMOX2). A CRISPR activation screen of 42 ATP-binding cassette (ABC) transporters, integrated with molecular docking and in vivo tumor imaging, identified ABCB1 as the primary efflux transporter regulating TiNIR distribution. These findings demonstrate a dual mechanism of probe selectivity: a binding-dependent pathway mediated by HMOX2 (Holding-Oriented Live-cell Distinction, HOLD) and a transporter-mediated efflux pathway via ABCB1 (Gating-Oriented Live-cell Distinction, GOLD). ABCB1 overexpression reduced TiNIR retention in non-target cells, whereas pharmacological inhibition or gene knockdown restored intracellular accumulation and significantly enhanced tumor signal intensity in mouse xenograft models. Molecular modeling confirmed TiNIR-ABCB1 interactions, supporting transporter-mediated probe clearance. Collectively, these findings establish TiNIR as a dual-mode molecular imaging probe and identify ABCB1 as a key determinant of probe selectivity in heterogeneous tumors. By integrating target binding with transporter efflux, TiNIR enables selective visualization of TICs and provides a framework for designing next-generation probes that overcome resistance-associated barriers in cancer diagnostics and theranostics. - Source: PubMed
Publication date: 2026/01/09
Ramos Sonny CLee Yong-AnMun Seul-KiMiyamoto NaokiSim Hyun BoLee Ju-BinHan Ji YeonWuestefeld TorstenLek Chee Chong JonathanChung Ho SeokJang Ji-HunJeong Seung-HyunChang Young-TaeKim Jong-Jin