Ask about this productRelated genes to: PDCD2 antibody
- Gene:
- PDCD2 NIH gene
- Name:
- programmed cell death 2
- Previous symbol:
- -
- Synonyms:
- ZMYND7, RP8
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-03
- Date modifiied:
- 2019-02-01
Related products to: PDCD2 antibody
Related articles to: PDCD2 antibody
- Programmed cell death 2 (PDCD2) is an evolutionarily conserved protein essential for cell viability from yeast to humans. PDCD2 functions as a dedicated chaperone to the 40S ribosomal protein uS5, and loss of PDCD2 function impairs ribosome biogenesis. As cancer cells require a substantial supply of ribosomes to maintain elevated levels of protein synthesis, targeting the protein interaction interface between PDCD2 and uS5 is a promising modality to mitigate ribosome biogenesis. In this study, we used affinity purification assays and structural modeling to identify a stretch of 30 amino acids in the N-terminal region of uS5 that is necessary and sufficient for interaction with PDCD2. Our data also identified a conserved FxxGFG motif in uS5 that is important for association with PDCD2 via hydrophobic interactions. Notably, we developed a sensitive complementation-based biosensor that can monitor PDCD2-uS5 interaction in cell extracts and living human cells. Using this biosensor, we identified an 11-amino acid uS5-derived peptide that inhibits the PDCD2-uS5 interaction and impairs cancer cell viability. Such peptides provide a starting point in the development of peptidomimetic inhibitors capable of modulating ribosome biogenesis via disruption of ribosomal protein-dedicated chaperone complexes. - Source: PubMed
Publication date: 2026/03/31
Mir Hassani ZabihGoulet FrédériqueNguyen Duc TaiLandry-Voyer Anne-MarieKwiatek LaurenGaudet ShanyBoudreault Pierre-LucAzad TahaBachand François - BackgroundGastric cancer is the 4th most common and 3rd deadliest cancer worldwide. Research has shown that PDCD2-like (PDCD2L) is elevated in several tumors.ObjectiveTo explore the relationship between PDCD2L expression and gastric cancer prognosis and its function in gastric cancer.MethodsImmunohistochemical staining and immunoblotting were performed to examine the expression of PDCD2L. The effect of PDCD2L on gastric cancer cells were evaluated by a series of in vitro cellular function experiments and in vivo proliferation experiments.ResultsPDCD2L was found to be overexpressed in gastric cancer tissues compared to non-tumor tissues, and its higher levels were associated with worse prognosis. In vitro experiments showed that reducing PDCD2L expression in gastric cancer cells led to decreased proliferation, migration, and invasion, with a similar effect observed in animal models. Knockdown of PDCD2L also resulted in lower expression of cell cycle- and motility-related proteins, while upregulation of PDCD2L had the opposite effect. Additionally, NGS analysis revealed that PDCD2L knockdown reduced the expression of RFX1, a gene linked to cell proliferation and migration, suggesting that PDCD2L and RFX1 together promote cancer progression.ConclusionPDCD2L could serve as a biomarker for gastric cancer prognosis and a potential therapeutic target. - Source: PubMed
Publication date: 2025/09/02
Sun Ding-PingChang Chun-ChaoHuang Hsuan-YiKang Nai-WengHseu You-ChengTian Yu-FengFang Chia-LangLin Kai-Yuan - Pregnancy loss is a major problem in clinical medicine with devastating consequences for families. Next generation sequencing has improved our ability to identify underlying molecular causes, though over half of all cases lack a clear etiology. Here, we began with clinical evaluation combined with exome sequencing across independent families to identify bi-allelic candidate genetic variants in the gene in multiple fetuses with nonimmune hydrops fetalis (NIHF). PDCD2 is an evolutionarily conserved protein with no prior association with monogenic disorders. PDCD2 is known to act as a molecular chaperone for the ribosomal protein uS5, and this complex formation is important for incorporation of uS5 into the 40S subunit, a crucial step in ribosome biogenesis. Primary fibroblasts from an affected fetus and cell lines expressing patient variants demonstrated reduced levels of PDCD2, reduced PDCD2 binding to uS5, and altered ribosomal RNA processing. tadpoles with Pdcd2 knockdown demonstrated developmental defects and edema, reminiscent of the NIHF seen in affected fetuses, and showed altered ribosomal RNA processing. Through genetic, biochemical, and in vivo approaches, we provide evidence that bi-allelic variants cause an autosomal recessive ribosomal biogenesis disorder resulting in pregnancy loss. - Source: PubMed
Publication date: 2025/04/10
Landry-Voyer Anne-MarieHolling TessMis Emily KMir Hassani ZabihAlawi MalikJi WeizhenJeffries LaurenKutsche KerstinBachand FrançoisLakhani Saquib A - : Unregulated post-prandial dietary endotoxemia may accumulate over time and underlie the development of chronic disease (e.g., leaky gut, inflammatory bowel disease, etc.), for which oral probiotic supplementation may be a prophylactic. The purpose of this study was to determine if 45 d of oral spore-based probiotic supplementation altered gastrointestinal-associated mRNA expression following a high-fat meal. : A subset of apparently healthy individuals from a larger study who had dietary endotoxemia at baseline completed 45 d of supplementation with either a placebo (rice flour; = 10) or spore-based probiotic (Megasporebiotic™; Novonesis, Kongens Lyngby, Denmark; (HU36™), (HU58™), (SC208™), and (SL-307), and (SC109™); = 10). Venous blood was collected in Paxgene RNA tubes prior to (PRE), 3 h, and 5 h after consumption of a high-fat meal (85% of the daily fat RDA and 65% of the daily calorie needs). Total RNA was analyzed for 579 mRNAs of interest (Nanostring nCounter Sprint; Seattle, WA, USA). After normalization to housekeeping controls and calculation of differential expression relative to PRE and controlled for FDR, 15 mRNAs were determined to be significantly changed at either 3 h and/or 5 h post-prandial in the probiotic group but not in the placebo group. : Significant mRNA expressions were associated with gastrointestinal tract barrier function (four mRNAs: BATF3, CCR6, CXCR6, and PDCD2), gastrointestinal immunity (four mRNAs: CLEC5A, IL7, CARD9, and FCER1G), or future IBD risk (seven mRNAs: PD-L1, CSF1R, FAS, BID, FADD, GATA3, and KIR3DL). : Collectively, the present findings may support the notion that post-prandial immune response to eating is enhanced following 45 d of probiotic supplementation. - Source: PubMed
Publication date: 2024/10/18
McFarlin Brian KDeemer Sarah EBridgeman Elizabeth A - Translation, a fundamental process regulating cellular growth and proliferation, relies on functional ribosomes. As sessile organisms, plants have evolved adaptive strategies to maintain a delicate balance between growth and stress response. But the underlying mechanisms, particularly on the translational level, remain less understood. In this study, we revealed the mechanisms of AtPRMT3-RPS2B in orchestrating ribosome assembly and managing translational regulation. Through a forward genetic screen, we identified PDCD2-D1 as a suppressor gene restoring abnormal development and ribosome biogenesis in atprmt3-2 mutants. Our findings confirmed that PDCD2 interacts with AtPRMT3-RPS2B, and facilitates pre-ribosome transport through nuclear pore complex, finally ensuring normal ribosome translation in the cytoplasm. Additionally, the dysfunction of AtPRMT3-RPS2B was found to enhance freezing tolerance. Moreover, we revealed that AtPRMT3-RPS2B promotes the translation of housekeeping mRNAs while concurrently repressing stress-related mRNAs. In summary, our study sheds light on the regulatory roles of AtPRMT3-RPS2B in ribosome assembly and translational balance, enabling the trade-off between growth and stress. - Source: PubMed
Publication date: 2024/10/08
Wang ZhenZhang XiaofanLiu ChunyanDuncan SusanHang RunlaiSun JingLuo LilanDing YiliangCao Xiaofeng