Ask about this productRelated genes to: EIF3S12 antibody
- Gene:
- EIF3K NIH gene
- Name:
- eukaryotic translation initiation factor 3 subunit K
- Previous symbol:
- EIF3S12
- Synonyms:
- eIF3k, PRO1474, HSPC029, PTD001, PLAC-24, M9, ARG134
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-10
- Date modifiied:
- 2015-12-04
Related products to: EIF3S12 antibody
Related articles to: EIF3S12 antibody
- Eukaryotic translation initiation factor 3 (eIF3) is a complex of proteins that plays a pleiotropic role in translation regulation across eukaryotes, but the composition of eIF3 complexes varies with retention and loss of subunit genes across evolution. The model yeast encodes six eIF3 subunits whereas mammals encode thirteen subunits. The basidiomycete fungus and opportunistic fungal pathogen, , encodes a mammalian complement of eIF3 subunits. In this report, we investigated the contribution of the non-essential eIF3 subunit genes to cryptococcal stress tolerance. We found that mutants in the four nonessential subunits, eIF3d, eIF3e, eIF3k and eIF3l all exhibit sensitivity to mitochondrial perturbation, and that mutants in eIF3d and eIF3e exhibit opposite susceptibilities to the antifungal drug fluconazole and the hypoxia mimetic cobalt chloride. Loss of eIF3d resulted in reduced eIF2α phosphorylation in response to stress, but the mutant was still able to repress translation to the same extent as the wild type and was defective in induction of integrated stress response regulon. Despite producing higher levels of urease and melanin, the eIF3d deletion mutant was avirulent in larvae. Together our data demonstrates the importance of eIF3 in stress adaptation and pathogenesis. - Source: PubMed
Publication date: 2026/01/12
Ventura Maritza NSingh PrabhakarGoich DavidPanepinto John C - Lipid droplet autophagy (lipophagy) is the breakdown and recycling of lipids within cells via autophagy. Some research suggests that enhancing lipophagy could have potential benefits for bone health. This study aimed to determine the key genes linked to lipophagy in osteoporosis (OP) and provided a reference for the treatment of OP. - Source: PubMed
Publication date: 2025/07/22
Hu YixinZuo MingliangWu YuYang YuShi XiaobingZhang QianWu JiXie RunqiBi YuLin BoMo Chou - We report two rare homozygous variants, including a recurrent missense and intronic variant, in the EIF3K gene in four unrelated individuals with global developmental delay, microcephaly, proportionate short stature, dysmorphic craniofacial features, digit flexion deformities, and the cardiac anomaly, patent ductus arteriosus. Three individuals, who were all of Puerto Rican descent, were homozygous for the NM_013234.3:c.128A>G; p.(Asp43Gly) variant in EIF3K and homozygous for a missense variant in SYNE4 (NM_001039876.2:c.355C>T; p.(Arg119Trp)). SYNE4 is associated with autosomal recessive bilateral sensorineural hearing loss, which was also reported in these probands. Analysis of our dataset confirmed these EIF3K and SYNE4 variants were in linkage disequilibrium in affected individuals, suggesting a possible common ancestor and founder event. A fourth individual from Egypt harbored the homozygous intronic variant c.355-13A>G in EIF3K, which segregated with the phenotype in the family and led to aberrant splicing of EIF3K pre-mRNAs, as shown by insertion of 12 intronic base pairs, skipping of 2 exons, and significantly reduced EIF3K protein levels in skin fibroblasts. Through genetic and functional approaches, we suggest that biallelic EIF3K variants are associated with an autosomal recessive syndromic neurodevelopmental disorder with growth retardation, microcephaly, congenital heart defect, and other anomalies. - Source: PubMed
Publication date: 2025/04/11
McGivern BobbiHolling TessGuillen Sacoto Maria JGudbjartsson HákonAbdelrazek Ibrahim MAlawi MalikBai YanBodamer OlafCrunk AmyDameron Amy EDyer Lisa MHenderson Lindsay BIrons MiraKutsche KerstinMcGowan CarolineMonaghan Kristin GO'Connor KaitlynRashid AsmaRedlich Olivia LReich AdiSimotas ChristopherWelner SaraWentzensen Ingrid M - Diabetic nephropathy affects a significant proportion of individuals with diabetes, and its progression often leads to cardiovascular disease and infections before the need for renal replacement therapy arises. Empagliflozin has been shown to have various protective effects in cardiovascular disease studies, such as improving diabetic myocardial structure and function, and reducing myocardial oxidative stress. However, the impact of empagliflozin on cardiac protein expression and signaling pathways has not been comprehensively analyzed. To address this gap, we conducted proteome analysis to identify specific protein markers in cardiac tissue from the diabetes model group, including Myh7, Wdr37, Eif3k, Acot1, Acot2, Cat, and Scp2, in cardiac tissue from the diabetes model group. In our drug model, empagliflozin primarily modulates the fat-related metabolic signaling pathway within the heart. Empagliflozin downregulated the protein expression levels of ACOX1, ACADVL and CPT1A in the model group. Overall, our findings demonstrate that empagliflozin provides cardiac protection by targeting metabolic signaling pathways, particularly those related to fat metabolism. Moreover, the identification of cardiac biomarkers in a mouse model of diabetic nephropathy lays the foundation for further exploration of disease biomarkers in cardiac tissue. - Source: PubMed
Publication date: 2024/10/19
Yu ZongchaoLu YongpingZhang MengxianLin YanshanWong Tak-SuiGuan BaozhangMeng YuHu BoLiu Fan-NaYin LianghongLi YankunZhang HanTang DongeDai Yong - Despite their role as innate sentinels, macrophages can serve as cellular reservoirs of chikungunya virus (CHIKV), a highly-pathogenic arthropod-borne alphavirus that has caused large outbreaks among human populations. Here, with the use of viral chimeras and evolutionary selection analysis, we define CHIKV glycoproteins E1 and E2 as critical for virion production in THP-1 derived human macrophages. Through proteomic analysis and functional validation, we further identify signal peptidase complex subunit 3 (SPCS3) and eukaryotic translation initiation factor 3 subunit K (eIF3k) as E1-binding host proteins with anti-CHIKV activities. We find that E1 residue V220, which has undergone positive selection, is indispensable for CHIKV production in macrophages, as its mutation attenuates E1 interaction with the host restriction factors SPCS3 and eIF3k. Finally, we show that the antiviral activity of eIF3k is translation-independent, and that CHIKV infection promotes eIF3k translocation from the nucleus to the cytoplasm, where it associates with SPCS3. These functions of CHIKV glycoproteins late in the viral life cycle provide a new example of an intracellular evolutionary arms race with host restriction factors, as well as potential targets for therapeutic intervention. - Source: PubMed
Publication date: 2024/09/11
Yao ZhenlanRamachandran SangeethaHuang SerinaKim ErinJami-Alahmadi YasamanKaushal PrashantBouhaddou MehdiWohlschlegel James ALi Melody M H