Ask about this productRelated genes to: Pnrc2 Blocking Peptide
- Gene:
- PNRC2 NIH gene
- Name:
- proline rich nuclear receptor coactivator 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-25
- Date modifiied:
- 2015-11-23
Related products to: Pnrc2 Blocking Peptide
Related articles to: Pnrc2 Blocking Peptide
- Decapping is a critical step in mRNA decay, but the mechanisms regulating human decapping enzyme DCP2 remain poorly understood. Here, we reconstitute the human decapping network using full-length recombinant proteins and compare it to the yeast system. Unlike in yeast, we find that the C-terminal region of human DCP2 is not autoinhibitory. RNA-binding residues of yeast Dcp2 are not conserved in the human homolog, and we find instead that a charged C-terminal region mediates substrate recognition. Human DCP1 does not stably interact with or directly stimulate DCP2, but mediates activation by the enhancer PNRC2. We also demonstrate that decapping enhancer EDC4 forms tetramers through an extended coiled-coil region, and that both DCP1 and EDC4 homomeric species can further assemble into higher-order oligomers. Furthermore, structural predictions incorporating these findings suggest a model for DCP2 recruitment by EDC4 tetramers. These findings reveal key mechanistic differences between human and yeast decapping regulation and provide insight into the molecular architecture underlying mRNA decay. - Source: PubMed
Publication date: 2026/04/21
Simko Eric A JMuthukumar SowndaryaMyers Tanner MValkov Anna LValkov Eugene - Somitogenesis, the sequential segmentation of vertebrate embryonic mesoderm, is controlled by the segmentation clock, a molecular oscillator that controls periodic gene expression in unsegmented mesoderm and is regulated by a negative feedback loop driven by Hes/Her transcriptional repressors. In zebrafish, Pnrc2 is required for decay of transcript and additional oscillatory gene transcripts. Despite accumulation of numerous mRNAs including those encoding key developmental regulators, overt embryonic phenotypes are absent in mutants. Our previous work suggested that accumulated mRNAs are not translated in mutants, though the underlying mechanism(s) was unknown. We show here that many overexpressed transcripts in mutants have shortened poly(A) tails and are disengaged from ribosomes, and that deadenylation inhibition leads to somite defects in mutants. In contrast, transcripts encoding the P-body protein, Ddx61, are both overexpressed and engaged with ribosomes, leading to an increase in Ddx61 protein. Co-depletion of Ddx61 and its ohnolog Ddx6 enhances accumulation and later leads to strong morphological defects in mutants. Together, our results show that multiple post-transcriptional mechanisms ensure proper translation when mRNA decay is inhibited. - Source: PubMed
Publication date: 2025/05/14
Gallagher Thomas LeeBlatnik Monica CAustin Clare CThompson Kathryn GPvirre Danielle MMorgan AngelinaKearse Michael GAmacher Sharon L - Long non-coding RNA (lncRNA) zinc finger protein 667-antisense RNA 1 () is closely related to the advancement of a variety of cancers, but its functional role in colorectal cancer remains unclear. This study was designed to explore the function and molecular mechanisms of lncRNA in colorectal cancer. - Source: PubMed
Li HaiqiangShen XuningLi Yan - - Source: PubMed
Publication date: 2024/07/05
Quan JingPan XiangLi YawenHu YiminTao LingzhiLi ZuweiZhao LiwenWang JingyaoLi HangLai YulinZhou LiangLin CanbinGui YaotingYe JingZhang FangtingLai Yongqing - Meningioma was the most primary intracranial tumor, but the molecular characteristics and the treatment of malignant meningioma were still unclear. Nine malignant progression-related genes based prognostic signatures were identified by transcriptome analysis between benign meningioma and malignant meningioma. The external dataset GEO136661 and quantitative Real-time Polymerase Chain Reaction were used to verify the prognostic factors. has-miR-3605-5p, hsa-miR-664b-5p, PNRC2, BTBD8, EXTL2, SLFN13, DGKD, NSD2, and BVES were closed with malignant progression. Moreover, Doxorubicin was identified by Connectivity Map website with the differential malignant progression-related genes. CCK-8 assay, Edu assay, wound healing assay, and trans-well experiment were used to reveal that Doxorubicin could inhibit proliferation, migration and invasion of IOMM-Lee Cells. - Source: PubMed
Publication date: 2023/04/06
Huo XuleiSong LairongWang KeWang HongyiLi DaLi HuanWang WeiWang YaliChen LeiZhao ZongmaoWang LiangWu Zhen