Ask about this productRelated genes to: MTCH2 antibody
- Gene:
- MTCH2 NIH gene
- Name:
- mitochondrial carrier 2
- Previous symbol:
- -
- Synonyms:
- SLC25A50
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-20
- Date modifiied:
- 2014-11-19
Related products to: MTCH2 antibody
Related articles to: MTCH2 antibody
- Triple-negative breast cancer (TNBC) represents a particularly aggressive form of breast tumors. Mitochondrial dysfunction represses the proliferation of TNBC cells. Ubiquitin-specific proteases 34 (USP34) has been predicted to be abnormally overexpressed in TNBC. This research examined the role of USP34 in the mitochondrial function modulation of TNBC. Herein, cell proliferation was evaluated by the 5-ethynyl-2'-deoxyuridine assay. Mitochondrial membrane potential was detected employing the JC-1 assay. Mitochondrial superoxide was measured utilizing MitoSOX Red assay. Mito‑Tracker Red CMXRos staining was selected to monitor mitochondrial network structure. The relationship among USP34, eukaryotic translation initiation factor 3 m (eIF3m), and mitochondrial carrier homolog 2 (MTCH2) was validated by co-immunoprecipitation, GST-pull down, RNA immunoprecipitation and RNA-pull down analysis. We found that USP34 silencing inhibited cell proliferation by inducing mitochondrial dysfunction in TNBC cells. USP34 maintained the stability of the eIF3m protein through deubiquitination. Overexpression of eIF3m countered the mitochondrial dysfunction induced by USP34 silencing. Furthermore, eIF3m upregulated the MTCH2 level by directly binding to its 5'UTR region. MTCH2 overexpression reversed the damaging effect of eIF3m silencing on mitochondrial function. Collectively, USP34 maintained the stability of eIF3m protein through deubiquitination; the upregulated eIF3m bound to the 5'UTR of MTCH2 mRNA to promote MTCH2 expression, thereby maintaining mitochondrial function and promoting the malignant progression of TNBC. - Source: PubMed
Publication date: 2026/04/23
Qian Peng-FeiZeng YiZhong Wang-Jing - Inflammation is associated with various cancers, including colorectal cancer. Momordin Ic (MIc) has anti-tumor and anti-inflammatory properties, but its effects on colitis-associated colorectal cancer (CAC) are not well understood. This study explores MIc's influence on macrophage mitochondrial dysfunction, macrophage polarization, and tumor development in CAC. Mouse colitis and CAC models were established to assess MIc's therapeutic potential. H&E staining and immunohistochemistry evaluated inflammation and mucosal damage in colonic tissues. Flow cytometry analyzed immune cell proportions, while Western blot analyzed inflammatory protein expression. In vitro studies with RAW264.7 and BMDMs explored MIc's effects on macrophage polarization and mitochondrial function. Flow cytometry assessed CD86+ macrophages, and qRT-PCR measured inflammatory cytokines. Mitochondrial function was assessed using Mito-tracker, JC-1, and DCFH-DA dyes. Proteomics and GO analysis identified downstream pathways. Flow cytometry and CCK-8 assessed colon cancer cell proliferation and apoptosis, confirmed in the CAC mouse model. MIc significantly reduced intestinal inflammation and mucosal damage by decreasing macrophage infiltration and pro-inflammatory polarization. Proteomics revealed that MIc affected proteins related to mitochondrial function. MIc restored mitochondrial function impaired by M1 polarization through upregulation of MTCH2. Co-IP analysis showed a direct interaction between Sentrin-specific protease 1 (SENP1) and MTCH2. SENP1 levels increased in M1 macrophages but decreased with MIc, an effect blocked by NFκB inhibitors. MIc promoted apoptosis in CT26 and HCT116 cells and inhibited CAC progression. MIc effectively suppresses CAC development by regulating macrophage mitochondrial function via the SENP1/MTCH2 pathway, reducing M1 polarization and promoting apoptosis in colorectal cancer cells. - Source: PubMed
Publication date: 2026/04/20
Xianjun FangChi ZhaiHaixia YuYu ChenKanghui FangWan HuangXingjian ZhangZude ChangYunxin LiuXi Cao - Roux-en-Y gastric bypass (RYGB) is a highly effective intervention for morbid obesity; however, significant inter-individual variability in long-term weight outcomes and the phenomenon of weight regain remain clinical challenges. Understanding the genetic and dietary factors influencing these variable responses is crucial for personalized patient management. - Source: PubMed
Publication date: 2026/03/25
Pires Izabella FerreiraPinhel Marcela Augusta de SouzaWatanabe Ligia MoriguchiDiani Luisa MariaSalgado-Júnior WilsonJulio Maysa de Araujo FerreiraFernandes Rafael FerreiraNoronha Natalia YNonino Carla B - Long noncoding RNAs (lncRNAs) are critical regulators of immune responses and cellular metabolism. Here, we report a previously unrecognized interaction between and HADHB, which reveals additional regulatory roles for in human macrophages. Our findings demonstrate that -HADHB interaction significantly enhances HADHB thiolase activity during the late phase of inflammation via HuR-MTCH2-mediated mitochondrial targeting of . also negatively regulates the pro-inflammatory macrophage activation via HADHB. Knockdown of induces metabolic reprogramming, characterized by enhanced glycolysis, increased fatty acid synthesis, and reduced fatty acid oxidation, suggesting that suppresses inflammatory metabolic pathways. This study uncovers the -HADHB interaction and demonstrates that regulates macrophage metabolic reprogramming, offering new insights into the metabolic control of inflammation and highlighting as a potential therapeutic target for inflammatory diseases. - Source: PubMed
Publication date: 2026/02/20
Liu YuxiangNakayama YukiteruSugita JunichiOshima TsukasaKani KunihitoKobayashi AtsushiSetoguchi NaotoIwai YoshikoManabe IchiroFujiu Katsuhito - Mitochondria orchestrate energy conversion and cell fate, yet label-free approaches that report both functional and physical states at the single-organelle level are nonexistent. Here, we combine atomic force microscopy (AFM) imaging with single-mitochondrion phenotyping by quantifying stiffness, height, and spontaneous low-frequency height fluctuations at the nanoscale. Across respiratory activators, inhibitors, and uncouplers, the integrated 0- to 20-Hz fluctuation power correlates with mitochondrial membrane potential (ΔΨ) and does not covary with changes in mitochondrial height (a proxy for swelling). In liver mitochondria lacking mitochondrial carrier homolog 2 (MTCH2), a regulator of mitochondrial metabolism, dynamics, and apoptosis, AFM reveals a compact, mechanically stiff, high-fluctuation state consistent with hyperpolarization and distinct from inhibited/uncoupled signatures. Extending the assay to mitochondria isolated from mouse embryonic fibroblasts, AFM data can distinguish between genotypes: loss of the mitochondrial pro-fusion proteins mitofusin 1 or 2 ( or ) yields stiff, low-fluctuation mitochondria with reduced ΔΨ, whereas MTCH2 loss produces stiff, high-fluctuation, high-ΔΨ mitochondria. These three label-free features provide reproducible single-organelle "fingerprints" that resolve bioenergetic states and molecular defects and complement fluorescence and respirometry. - Source: PubMed
Publication date: 2026/03/05
Zorikova Ekaterina OChourasia SabitaRosenhek-Goldian IritCohen Sidney RNesterov Semen VGross Atan