B5 Receptor _ PCID1 _ EIF3M Antibody
- Known as:
- B5 Receptor _ PCID1 _ EIF3M Antibody
- Catalog number:
- AF1132a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- B5 Receptor _ PCID1 EIF3M Antibody
Ask about this productRelated genes to: B5 Receptor _ PCID1 _ EIF3M Antibody
- Gene:
- EIF3M NIH gene
- Name:
- eukaryotic translation initiation factor 3 subunit M
- Previous symbol:
- PCID1
- Synonyms:
- hfl-B5, FLJ29030, GA17, eIF3m, TANGO7
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-31
- Date modifiied:
- 2015-12-04
Related products to: B5 Receptor _ PCID1 _ EIF3M Antibody
Related articles to: B5 Receptor _ PCID1 _ EIF3M Antibody
- The reprogramming of myocardial energy metabolism is critical for cardiac repair after ischemia/reperfusion (I/R) injury, yet the upstream translational control mechanisms remain elusive. Here, through multi-omics analysis of human failing hearts, we identify the mRNA regulator eIF3m as an essential factor for maintaining cardiac glycolytic flux post-I/R. We show that eIF3m, independently of the canonical eIF3 complex, stabilizes Mt2 and related stress-response mRNAs, ultimately protecting the key glycolytic activator Pfkfb3. Loss of eIF3m impairs the heart's adaptive shift toward utilizing glycolysis for energy, leading to contractile dysfunction. Mechanistically, eIF3m deficiency exacerbates excessive nitro-oxidative stress, which damages and inactivates the key glycolytic enzyme Pfkfb3. This damage is counteracted by the metallothionein Mt2, a direct binding partner of eIF3m. Our findings reveal the eIF3m-Mt2 axis as a novel translational checkpoint that governs metabolic reprogramming and nitrative stress resistance in the injured heart, nominating it as a potential therapeutic target for myocardial I/R injury. - Source: PubMed
Publication date: 2026/08/08
Wei ZilunZhao YongchaoJia DaileGao RifengXiong WeidongSun XiaoleiWeng XinyuLiu BowenSong ShuaiLuo WeiCui JianHu KaiSun AijunGe Junbo - End-stage chronic liver disease in children is associated with sarcopenia and aberrant adipose tissue mass. We investigated correlations between liver pathology-associated gene pathways (fibrosis, inflammation and steatosis) and metabolic genes in muscle and adipose tissue. - Source: PubMed
Publication date: 2026/07/06
Kyrana EiriniZhang ChengJin HanSalehi SiamakWells Jonathan C KDeheragoda MaeshaMitry Ragai RDhawan Anil - 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 - Eukaryotic initiation factors (eIFs), a bunch of proteins that deeply involved in translation initiation of mRNA in eukaryotes, are closely associated with physiological and pathological processes. eIF3m, a core subunit in eIF3 complex, also played critical roles in virus infection. In this study, a co-immunoprecipitation coupled with mass spectrometry (Co-IP/MS) was performed to identify host factors that interacted with ORF1B, a unique non-structural protein of fowl adenovirus serotype 4 (FAdV-4). Among 2502 cellular proteins, eIF3m, especially its C-terminal part, was verified to interact with ORF1B and these two proteins co-localized in the cytoplasm. Importantly, overexpression of eIF3m promoted FAdV-4 replication in LMH cells, whereas knockdown eIF3m exerted an opposite effect. Collectively, these findings indicate that ORF1B hijacked eIF3m to positively participate in FAdV-4 infection. - Source: PubMed
Publication date: 2026/01/31
Wang ZengLi RuixueZhai SaiminGao HuichaoLiu KeyingYang XiaZhao JunZhang Xiaozhan - Italy hosts a rich heritage of poultry genetic resources, leading to the development of several unique native chicken breeds. Among them, the Leccese (LEC) chicken breed requires urgent genetic characterization to support conservation, development, and sustainable use. This study assessed the genetic diversity and population structure of the LEC chicken breed using the 600 K Affymetrix SNP array, comparing it with 25 Italian indigenous breeds and four commercial lines. In addition, selection signatures were explored through runs of homozygosity and integrated haplotype score analyses. The observed heterozygosity, expected heterozygosity, and minor allele frequency in LEC were 0.343, 0.358, and 0.268, respectively. The inbreeding coefficient based on observed versus expected homozygosity was 0.044, and the inbreeding coefficient based on runs of homozygosity was 0.189. Population structure analyses revealed clear genetic differentiation between the LEC and other Italian chicken breeds. Selective sweep analyses (runs of homozygosity and integrated haplotype score) identified candidate genomic regions harboring genes related to growth (GBE1, CYFIP1, NIPA2, BBOX1), bone development (PHEX), disease resistance (ROBO2, TLR7, EIF3M), and environmental adaptation (ANO5, CCDC34, HSF4, SPON1). These findings provide novel insights into the genetic background of the LEC, supporting breed identification, conservation planning, and the design of sustainable breeding programs. The identified candidate genes within selective sweep regions may serve as markers for future selection to enhance productive traits and adaptation in the LEC chicken breed. - Source: PubMed
Publication date: 2025/12/13
Saleh Medhat SRusco GiusyCendron FilippoPerini FrancescoPenasa MauroLasagna EmilianoCentoducati GerardoMaggiolino AristideCassandro MartinoCamarda AntonioDe Palo PasqualeLandi Vincenzo