Rnf14 antibody - N-terminal region (ARP33724_P050)
- Known as:
- Rnf14 (anti-) - N-terminal region (ARP33724_P050)
- Catalog number:
- arp33724_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Rnf14 antibody - N-terminal region (ARP33724_P050)
Related genes to: Rnf14 antibody - N-terminal region (ARP33724_P050)
- Gene:
- RNF14 NIH gene
- Name:
- ring finger protein 14
- Previous symbol:
- -
- Synonyms:
- ARA54, HFB30, TRIAD2
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-14
- Date modifiied:
- 2016-10-05
Related products to: Rnf14 antibody - N-terminal region (ARP33724_P050)
Related articles to: Rnf14 antibody - N-terminal region (ARP33724_P050)
- Amino acids can become limiting for protein synthesis through depletion of charged tRNAs, leading to ribosome stalling and disruption of translation elongation at specific codons. To assess whether this is a mechanism by which amino acid availability can directly influence gene expression, we designed a reporter library to measure translation disruption across all sense codons in the context of amino acid limitations. We found that arginine limitation consistently impairs translation at the arginine codon AGA, resulting in synthesis of proteins from endogenous transcripts. In contrast, GCN2 pathway activation suppresses translation disruption following depletion of most other amino acids. Genome-wide screens revealed that the ribosome quality control trigger (RQC-T) and RQC pathways, which resolve ribosome collisions on defective mRNAs, catalyze ribosome splitting and premature fall-off in response to arginine depletion. Additionally, the E3 ubiquitin ligase RNF14, recently shown to clear ribosome A-site obstructions, promotes translation disruption through both ribosome fall-off and frameshifting during arginine limitation. Together, these data show that the RQC machinery is engaged by tRNA-limited ribosomes and identify a new role for RNF14 as a regulator of translation upon arginine limitation. - Source: PubMed
Publication date: 2026/01/15
Darnell Alicia MChidley ChristopherParadise VictoriaCui Danica SDavidsen KristianLincoln Sarah CAbbott Keene LElbashir RyanVander Heiden Campbell PSorger Peter KSullivan Lucas BDavis Joseph HVander Heiden Matthew G - E3 ligases partner with E2 enzymes to regulate vast eukaryotic biology. The hierarchical nature of these pairings, with >600 E3s and ~40 E2s in humans, necessitates that E2s cofunction with numerous different E3s. Here, focusing on E3s in the RING-between-RING (RBR) family and their partner UBE2L3 and UBE2D-family E2s, we report an approach to interrogate selected pathways. We screened phage-displayed libraries of structure-based E2 variants (E2Vs) to discover enzymes with enhanced affinity and specificity toward half of all RBR E3 ligases (ARIH1, ARIH2, ANKIB1, CUL9, HOIL1, HOIP, and RNF14). Collectively, these E2Vs allowed distinguishing actions of different cofunctioning E3s, obtaining high-resolution cryogenic Electron Microscopy (cryo-EM) structures of an RBR E3 in the context of a substrate-bound multiprotein complex, and profiling an endogenous RBR E3 response to an extracellular stimulus. Overall, we anticipate that E2V technology will be a generalizable tool to enable in-depth mechanistic and structural analysis of E3 ligase functions, and mapping their activity states and protein partners in cellular signaling cascades. - Source: PubMed
Publication date: 2026/01/02
Du JialeAndree Gisele AHorn-Ghetko DanielStier LucaSingh JaspalKostrhon SebastianKiss LeoMann MatthiasSidhu Sachdev SSchulman Brenda A - Hypopituitarism is a severe endocrine disorder characterized by a partial or complete hormone deficiency in the anterior or posterior pituitary gland. Current treatment relies on hormone replacement therapy, which is unable to mimic normal physiological circadian rhythm precisely, and long-term hormone replacement therapy can result in a variety of adverse effects. This study aimed to identify potential drug targets and clarify the mechanisms underlying hypopituitarism. To identify potential therapeutic targets for hypopituitarism, summary statistics from expression quantitative trait loci (eQTL) datasets, serum and cerebrospinal fluid (CSF) metabolites, and hypopituitarism genome-wide association study (GWAS) data were integrated for analysis. Two-sample Mendelian randomization (MR) analysis was performed to identify causal genes associated with hypopituitarism. Subsequently, the relationship between serum and CSF metabolites and hypopituitarism was investigated. Finally, a two-step MR analysis explored the mediation of these metabolites in the causal gene-hypopituitarism pathway, quantifying both direct and mediation effects. A total of 20 genes associated with hypopituitarism were identified, with RMI2, UBAC1, and GLIPR1 further validated by Bayesian colocalization, and the causal relationship between CHST13, GABPB1-AS1, GLIPR1L2, RNF14, and hypopituitarism was confirmed by summary data-based MR (SMR) and HEIDI analysis. Additionally, 34 serum metabolites and 8 CSF metabolites were causally associated with hypopituitarism. Furthermore, mediation MR analysis demonstrated that 1-Methyl-4-imidazoleacetate was the only mediator, explaining 4.35% (P = 0.049) of the total effect of UBAC1 on increased hypopituitarism susceptibility. This study identified RMI2, UBAC1, CHST13, GABPB1-AS1, GLIPR1L2, RNF14, and GLIPR1 as potentially causal genes in the pathogenesis of hypopituitarism. Furthermore, UBAC1-mediated regulation of serum metabolites may contribute to promoting hypopituitarism progression, indicating that UBAC1 is a candidate gene warranting further functional validation. Future directions could include assessing UBAC1 expression in pituitary/hypothalamus single-cell RNA-seq or in vivo models. - Source: PubMed
Publication date: 2025/11/13
Sun YeshengZhang YingLuan TengfeiLi RuichunCai DongpengZhang Wei - The present study aimed to explore runs of homozygosity (ROH), Heterozygosity Enriched Regions (HER) using the sliding window approach in both PLINK and detectRUNS, as well as the consecutive SNP approach in detectRUNS and their association with important economic traits. Genomic inbreeding coefficient based on ROH and heterosis coefficient based on HER were also estimated among crossbred (n = 81) by using GGP_HDv3_C genotyping assay. Total ROH varied from around 600 in the sliding window approach and almost double in the Consecutive SNP approach of detectRUNS. Similarly, the HER are 756 in the sliding window and 771 in the Consecutive SNP method. The mean inbreeding coefficient range varied in different approaches, i.e., 0.016-0.022 is observed based on ROH (Froh), and the heterosis coefficient based on HER (Frohet) is 0.0019. Top ROH and HER regions contain important genes related to dairy (EHHADH, CACNA1C, MICALL1, EIF3L, GTPBP1, SYNGR1, ATF4, GRAP2, FAM83F, ACO2), immunity (LIPH, TMEM41A, PEX26, CDC42EPI, CXXC5, PSD2, PURA, CYSTM1, RNF14), growth and carcass (MAGEF1, TGS1, LYN, CHCHD7, FAM110B, SDCBP, SH3BP1, GGA1, TRIOBP, PICK1, MAFF, TOMM22, MGAT3, TNRC6B, ADSL, EP300, SMDT1, MATR3) traits. These findings may provide valuable insights into the understanding of genome-wide homozygosity and heterozygosity patterns and genetic architecture of the Pakistani crossbred cattle. - Source: PubMed
Publication date: 2025/09/26
Nisa Fakhar UnUsman MuhammadAli AsadAli Muhammad BasilKaul HaibaAsif MuhammadMrode RaphaelMukhtar Zahid - Prostate cancer bone metastasis is a predominant cause of death for prostate cancer (PCa) patients. However, the underlying mechanisms are poorly understood. Here, we report that high levels of RNF41 are associated with metastatic human prostate cancer. RNF41 silencing inhibits prostate cancer cell growth, cell migration and invasion in vitro and in vivo. Mechanistically, we identify that RNF41 induces K27- and K63-linked noncanonical polyubiquitination of MYO1C to enhance its stability and induce actin remodeling, which promotes PCa bone metastasis. RNF41 was significantly upregulated in metastatic prostate cancer tissues and positively associated with MYO1C expression. Furthermore, we show in intraarterial injected-bone metastasis xenograft model that targeting MYO1C stability by inhibition of RNF41 markedly suppressed PCa bone metastasis. Collectively, our findings identify RNF41 is an important regulator of prostate cancer cell growth and metastasis and targeting RNF41/MYO1C could be a valuable strategy to ameliorate prostate cancer progression and metastasis. - Source: PubMed
Publication date: 2024/08/07
Xiong SituLi ShengLi ZhongqiSong YanpingYang LinYang HailangXiong JingPan WangGuo JuFu BinXu Songhui