Ask about this productRelated genes to: Eif1 antibody
- Gene:
- EIF1 NIH gene
- Name:
- eukaryotic translation initiation factor 1
- Previous symbol:
- -
- Synonyms:
- EIF-1, ISO1, A121, SUI1, EIF1A
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-03-04
- Date modifiied:
- 2015-09-11
Related products to: Eif1 antibody
Related articles to: Eif1 antibody
- The eukaryotic translation initiation is a biological process in which at least a dozen eukaryotic initiation factors (eIFs) are involved. Specifically, eIF3, eIF1, eIF5, and eIF2 as a ternary complex (eIF2-TC) bound to GTP and methionyl initiator tRNA (Met-tRNA ). They interact to form a large complex called the multifactor complex (MFC). This complex binds cooperatively to the ribosomal pre-initiation complex (PIC), promoting the loading of the Met-tRNA into the peptidyl (P) site of the 40S ribosomal subunit. While some interactions between eIFs have been described in the context of the PIC, the interactions within the MFC remain poorly understood. Here, we combine biophysical and biochemical approaches, including mass photometry and native mass spectrometry, with structural biology methods such as electron microscopy, to gain deeper insights into the MFC architecture. Our findings provide novel insights into the critical role of eIF5 during MFC assembly. Notably, two copies of eIF5 are involved in the formation of the MFC. We propose that one eIF5 molecule engages eIF2β and eIF2γ, whereas a second eIF5 molecule interacts with eIF1 together with eIF3c. - Source: PubMed
de la Fuente Borja SáezVillamayor-Belinchón LauraCiges-Tomas José RafaelLópez-Redondo MarisaEspinosa CarolinaBoeri Erba ElisabettaLlácer José L - Toxoplasma gondii is a globally prevalent protozoan parasite capable of establishing lifelong infections in its host. While acute infection is often asymptomatic, reactivation of latent bradyzoites can cause severe disease, particularly in immunocompromised individuals. Current therapies are ineffective against chronic infection, underscoring critical gaps in our understanding of bradyzoite biology and the molecular mechanisms governing stage conversion. Recent studies have identified translational control as a central regulator of T. gondii differentiation. This review highlights the roles of canonical translation initiation factors (eIF2α, eIF1.2, and eIF4E1), RNA-binding proteins (RBPs; BFD2/ROCY1, Alba1, and Alba2), and RNA modifications (with pseudouridylation representing the best-characterized modification currently linked to differentiation), as well as alternative splicing and non-coding RNAs in shaping stage-specific translational programs. This review further discusses underexplored mechanisms, including non-canonical initiation pathways, upstream open reading frames, transcript-level RNA modifications, ribosome heterogeneity and rRNA modifications, elongation and termination control, uncharacterized RBPs, and post-translational modifications of translation factors, that may coordinate proteome remodeling during differentiation. Together, established translational regulators and these emerging pathways highlight translational control as a central driver of parasite persistence and a promising therapeutic target for chronic toxoplasmosis. - Source: PubMed
Wang Fengrong - Gastric cancer (GC) is a highly aggressive malignancy with a poor prognosis, closely linked to the tumor microenvironment (TME). Emerging evidence highlights the critical role of gastric cancer-associated mesenchymal stem cells (GC-MSCs) in recruiting neutrophils and facilitating neutrophil extracellular traps (NETs) formation, thereby remodeling the tumor microenvironment (TME) and promoting tumor progression, immune modulation, and metastasis. - Source: PubMed
Publication date: 2025/11/20
Li ZhengruiLuo PengZhou ZhaokaiCao JijunZhang Wen - Plasmodium (P.) falciparum, the deadliest malaria-causing parasite, challenges eradication efforts due to drug resistance. The regulation of mRNA translation as a therapeutic target remains unexplored. Most mRNAs contain unusually long 5'UTR and multiple upstream AUGs. How the parasite overcomes scanning distance and multiple uORF constraints is unknown. We employed the eIF1-eIF4G1 inhibitor i14G1-12, Ribo-seq, TIS-seq, and long-read data on P. falciparum trophozoites. Re-annotation of 5'UTRs, initiation site mapping, and translation efficiency (TE) analysis revealed extended 5'UTR length in hundreds of genes and actively translated uORFs in 81% of mRNAs. Active uORFs were predominantly initiated with AUG lacking specific context, while inactive uORFs were enriched with inhibitory AUG contexts. Notably, initiation within coding sequence through leaky scanning is also highly prevalent. Surprisingly, mRNAs with long 5'UTR and active uORFs exhibit higher TE than those without. We demonstrate that this is facilitated by a specific spacing of active uORFs and peptide length, optimizing scanning distance, ribosome density, and reinitiation. Remarkably, short-term i14G1-12 treatment reduced parasite viability and caused translational repression by enhancing leaky scanning and disturbing the unique arrangement of uORFs. Collectively, our findings uncovered the unusual translation regulatory features of P. falciparum and highlighted the therapeutic potential of targeting these mechanisms. - Source: PubMed
Barzilay RomLev AnastasiaFraticelli DavideOgran ArielRojas AliciaAbou Karam PaulaRegev-Rudzki NetaDikstein Rivka - Nucleotide repeat expansions, such as the GGGGCC repeats in C9orf72, associated with C9-ALS, are linked to neurodegenerative diseases. These repeat sequences undergo a noncanonical translation known as repeat-associated non-AUG (RAN) translation. Unlike canonical translation, RAN translation initiates from non-AUG codons and occurs in all reading frames. To identify potential regulators of RAN translation, we employed a bottom-up approach using a human factor-based reconstituted cell-free translation system to recapitulate RAN translation. This approach revealed that omission of either eIF1A or eIF5B enhanced the translation in all reading frames of C9orf72-mediated RAN translation (C9-RAN), suggesting that eIF1A and eIF5B act as repressors of RAN translation. eIF1A and eIF5B are known to contribute to the fidelity of translation initiation. In HEK293T cells, double knockdown of eIF1A and eIF5B further promoted C9-RAN compared to single knockdowns, indicating that these factors regulate C9-RAN through distinct initiation steps. Furthermore, under eIF1A knockdown conditions, the enhancement of RAN translation via the integrated stress response (ISR) was not observed in HEK293T cells, indicating that eIF1A is involved in the ISR-mediated non-AUG translation. - Source: PubMed
Ito HayatoMachida KodaiFujino YuzoHasumi MayukaSakamoto SoyokaNagai YoshitakaImataka HiroakiTaguchi Hideki