4E_T _ EIF4ENIF1 Antibody
- Known as:
- 4E_T _ EIF4ENIF1 Antibody
- Catalog number:
- AF1002a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- 4E_T _ EIF4ENIF1 Antibody
Related genes to: 4E_T _ EIF4ENIF1 Antibody
- Gene:
- EIF4ENIF1 NIH gene
- Name:
- eukaryotic translation initiation factor 4E nuclear import factor 1
- Previous symbol:
- -
- Synonyms:
- 4E-T, FLJ21601, Clast4, 2610509L04Rik
- Chromosome:
- 22q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-06-18
- Date modifiied:
- 2016-10-05
Related products to: 4E_T _ EIF4ENIF1 Antibody
Related articles to: 4E_T _ EIF4ENIF1 Antibody
- Female reproductive aging is a continuum characterized by the depletion of ovarian follicles, including Early Menopause (EM) and Premature ovarian insufficiency (POI).POI exhibits a strong genetic predisposition. Eukaryotic Translation Initiation Factor 4E nuclear import factor 1 (EIF4ENIF1), a key regulator of gene expression, plays a crucial role in oocyte maturation and follicular development. Accumulating evidence indicates that functional abnormalities in EIF4ENIF1 are closely associated with the onset and progression of POI. Therefore, identifying pathogenic variants in EIF4ENIF1 is of significant importance for elucidating its pathogenic mechanisms in POI and advancing clinical diagnosis. - Source: PubMed
Publication date: 2026/07/22
Sun JiaqiLiu BoHu MengjiaoQi QiChen WenxinChen JianlinLiu ErkaiZeng JunLi LongfeiYe KunHuang Hualin - The maternal-to-zygotic transition (MZT) is essential for early embryonic development, comprising zygotic genome activation (ZGA) as well as the degradation of maternal RNAs and proteins, whereas our understanding of repressors' role in this process remains limited in mammals. In our study, we inhibited protein degradation at the 1-cell stage using the proteasome inhibitor MG132 and observed impaired pre-implantation development and defective ZGA. Proteomic analysis of MG132-treated embryos showed that significantly up-regulated proteins in abundance were enriched for RNA-binding proteins (RBPs). Further functional screening highlighted one critical factor, 4E-T (EIF4ENIF1), whose overexpression caused 2-cell stage arrest and failure of ZGA initiation. Moreover, the abnormal accumulation of 4E-T translationally repressed key factors of the 1-cell embryo, including ZBED3 and KDM4A. Mechanistically, the reprsssion is linked to direct interactions of 4E-T with eIF4E and eIF4E1B. These findings suggest that specific maternal RBPs may act as repressors that require precise degradation post-fertilization to relieve translational repression and ensure successful MZT. - Source: PubMed
Publication date: 2026/07/13
Wang PinhuaWang SiqiYin HaojieYe MaoshengLi MingruiZhou ShuaiWang YufengGuo YueshuaiJia LongfeiGuo XuejiangWang QiangHu YueHuo Ran - Defining how proteins change over developmental time is amenable to studies deciphering regulatory genetic networks in vertebrate development, biology, and pharmacology. In an approach toward such quantitative studies of dynamic network behavior, we produced an atlas using the mass spectrometry-based method to investigate protein expression changes across 16 time points from the zygote to the early pharyngula stage zebrafish embryos. We systematically summarize 8 clusters for interrogating changes in protein expression associated with the development of zebrafish embryos. Specifically, we identified a class of zinc finger-related transcription factors primarily located on the long arm of chromosome 4, which are highly expressed during zygotic genome activation. Furthermore, we highlight the power of this analysis to assign developmental stage-specific expression information to chromosomes and tissues. Time-resolved analyses reveal significant discordance between differential transcript and protein expression, whereas no time lag is observed for proteins involved in stable and fundamental biological processes, such as metabolism (e.g., Ppt2a and Gatm), cytoskeletal organization (e.g., Col18a1), and the translation machinery (e.g., Eif4enif1). This atlas offers high-resolution and in-depth molecular insights into zebrafish development, providing a resource for developmental biologists to generate hypotheses for functional analysis of proteins during early vertebrate embryogenesis. - Source: PubMed
Publication date: 2026/03/26
Fang FeiPoulos WilliamYue YifanLi KunCibelli Jose BLiu XiaowenSun Liangliang - Hematopoietic stem cells (HSCs) possess the ability to long term reconstitute all the blood lineages and generate all blood cell types. As such, the in vitro generation of HSCs remains a central goal in regenerative medicine. Despite many efforts and recent advancements in the field, there is still no robust, reproducible, and efficient protocol for generating bona fide HSCs in vitro. This suggests that certain regulatory elements have yet to be uncovered. Here, we present a novel and unbiased approach to identifying endogenous components to specify HSCs from pluripotent stem cells. We performed a genomewide CRISPR activator screening during mesodermal differentiation from mouse embryonic stem cells. After in vitro differentiation, mesodermal KDR+ precursors were transplanted into primary and secondary immunodeficient NSG mice. This approach led to the identification of 7 genes (Spata2, Aass, Dctd, Eif4enif1, Guca1a, Eya2, and Net1) that, when activated during mesoderm specification, induce the generation of hematopoietic stem and progenitor cells. These cells are capable of serial engraftment and multilineage output (erythroid, myeloid, and T and B lymphoid) in vivo. Single-cell RNA sequencing further revealed that activating these 7 genes biases the embryoid bodies toward intraembryonic development, instead of extraembryonic, increasing the number of mesodermal progenitors that can generate HSCs. Our findings underscore the importance of differentiation during the first germ layer specification to generate definitive blood stem cells. - Source: PubMed
Palma Luis GKartha Gayathri MMaqueda MariaBarrero MercedesCanton EricIglesias ArnauGonzález JessicaHerrero-Molinero PatriciaTorres-Ruiz RaúlPayer BernhardBueno ClaraMenéndez PabloEspinosa LluisBigas Anna - We created the c.1286C>G stop-gain mutation found in a family with primary ovarian insufficiency (POI) at age 30 years. The Eif4enif1 C57/Bl6 transgenic mouse model contained a floxed exon 10-19 cassette with a conditional knock-in cassette containing the c.1286C>G stop-gain mutation in exon 10. The hybrid offspring of CMV-Cre mice with Eif4enif1WT/flx mice were designated Eif4enif1WT/Δ for simplicity. A subset of female heterozygotes (Eif4enif1WT/Δ) had no litters. In those with litters, the final litter was earlier (5.4 ± 2.6 vs 10.5 ± 0.7 months; P = .02). Heterozygous breeding pair (Eif4enif1WT/Δ × Eif4enif1WT/Δ) litter size was 60% of WT litter size (3.9 ± 2.0 vs 6.5 ± 3.0 pups/litter; P < .001). The genotypes were 35% Eif4enif1WT/flx and 65% Eif4enif1WT/Δ, with no homozygotes. Homozygote embryos did not develop beyond the 4- to 8-cell stage. The number of follicles in ovaries from Eif4enif1WT/Δ mice was lower starting at the primordial (499 ± 290 vs 1445 ± 381) and primary follicle stage (1069 ± 346 vs 1450 ± 193) on day 10 (P < .05). The preantral follicle number was lower starting on day 21 (213 ± 86 vs 522 ± 227; P < .01). Examination of ribosome protected mRNAs demonstrated altered mRNA expression. The Eif4enif1 stop-gain mice replicate the POI phenotype in women based on an earlier end to reproduction due to oocyte loss. The unique mouse model provides a platform to study regulation of protein translation across oocyte and embryo development in mammals. - Source: PubMed
Moriwaki MikaLiu LihuaJames Emma RTolley Neal DO'Connor Ashley MEmery BenjaminAston Kenneth IvanCampbell Robert AWelt Corrine K