Ask about this productRelated genes to: LRDD antibody
- Gene:
- PIDD1 NIH gene
- Name:
- p53-induced death domain protein 1
- Previous symbol:
- LRDD, PIDD
- Synonyms:
- MGC16925, DKFZp434D229
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-04
- Date modifiied:
- 2014-11-18
Related products to: LRDD antibody
Related articles to: LRDD antibody
- The efficacy of radiofrequency ablation (RFA) is constrained by incomplete tumor ablation, particularly in cases of excessive tumor volume, leading to elevated recurrence rates. Elucidating the genetic and microenvironmental alterations following incomplete ablation is essential for improving therapeutic outcomes. We aimed to identify the tumor-intrinsic molecular link between residual tumor cells and the immunosuppressive microenvironment that drives recurrence after RFA. - Source: PubMed
Publication date: 2026/07/03
Lu XuXiong ZhiyongTang YongshengSong YingqiuYuan ZenanLi LingKang ManqiuHe XinQiao ZihanZhu ShuguangZhang QiWang TiantianLi HuaJia Changchang - Adenosine diphosphate (ADP) ribosylation (ADPr) regulates multiple stress responses, yet substrates in the apoptotic machinery remain elusive. We show that a single, DNA damage-induced ADPr event controls proapoptotic PIDDosome (PIDD1/RAIDD/caspase-2) formation in response to unresolved interstrand DNA cross-links (ICL). ADPr targets conserved E783 in the PIDD1 death domain (DD); is catalyzed by poly(ADP-ribose) polymerase 4 (PARP4), a phylogenetically orphan PARP of previously unknown function; is reversed by the ribosylhydrolase activity of PARP14; and is triggered by Ataxia Telangiectasia and RAD3-related (ATR) phosphorylation-induced, PIAS1-mediated SUMOylation of the PIDD1 DD, which enables PARP4 docking. PIDD1 ADPr is dispensable for the recruitments of RAIDD and caspase-2 but essential for the dimerization of the caspase. Hence, denying E783 ADPr spares the onset of PIDDosome assembly but blocks its completion, thus eliminating caspase-2 activation and ensuing apoptosis. Conversely, removal of PARP14 forces apoptosis, even in cells with tolerable damage. The data identify PARP4 as an ICL response effector and illuminate a three-step modification sequence of the PIDD1 DD that conducts PIDDosome assembly from initiation to completion. - Source: PubMed
Publication date: 2026/04/29
Shah Richa BLi YuanyuanPerson AshleyFrigon LéonieÐukić NinaKini ElaChen RaymondPascal John MCohen Michael SAhel IvanHaley John DSidi Samuel - The ISO 10993-5 recommends the cytotoxicity in vitro tests of the medical devices for the 2D cultures. The aim of the study was: - to develop the L929 cell cultures in the 3D model; - to adapt the above tests for the 3D L929 cell culture using the latex extracts; - to define how the model of the cell culture affect the response of the cells in terms of morphology, viability and the expression of Bax, Bcl2, Jkamp, Pidd1 and Cyp3a44 genes, and - to check whether this potential response depends on the cell age. To achieve these goals the optical and confocal microscopy, the LDH test and RT-qPCR technique were used. The L929 cells are relatively easy to culture in the 3D model The 103-105 cells/well were selected as optimal for the L929 spheroid formation. Generally, the 3D L929 cell cultures were less sensitive to the latex extracts than the 2D. The visible cytotoxic effects were noted regardless the age of cells, after 48 hrs. However, the spheroids of the older cells, after 72 hrs of exposure neutralized the cytotoxic effects and were regenerated. This effect was also confirmed in the LDH test and may be related to the high expression of the Bax gene.The expression of all analysed genes were changed in the 3D conditions. The cytotoxicity in vitro studies using the 3D model imposed certain limitations that are not present in the traditional model. Firstly, a limitation is the cell age, as the older L929 cells have been shown to be more sensitive to the cytotoxic agent. Secondly, for the older cells, a limitation may be the exposure time, given the potential for the spheroid regrowth. - Source: PubMed
Publication date: 2026/04/28
Gruber-Bzura BeataBubko IrenaMielczarek LidiaPogorzelska AnnaWiktorska Katarzyna - We recently identified variants in 10 genes that are members of either the p53 pathway or Fanconi Anemia Complex (FAC), regulators of DNA repair (DNA damage response [DDR]) in 17 cases with pediatric acute-onset neuropsychiatric syndrome (PANS) or regression in autism spectrum disorder and other neurodevelopmental disorders (NDD). We aimed to identify additional cases with genetic vulnerabilities in DDR and related pathways. - Source: PubMed
Publication date: 2026/02/09
Vettiatil DhanyaSoorajkumar AnjanaDubin Robert APedrosa Erika MSchornagel AllanLambert John SCosta Isadora PinheiroMcDonald JosephSwagemakers Sigrid M Avan der Spek Peter JFrankovich JenniferCunningham Janet LLachman Herbert M - The adult mammalian heart is characterized by post-mitotic polyploid cardiomyocytes (CMs). Understanding how CMs regulate cell cycle exit and polyploidy can help developing new heart regenerative therapies. Here, we uncover that the PIDDosome, a multi-protein complex activating the endopeptidase Caspase-2, helps to implement a CM-specific differentiation program that limits ploidy during postnatal heart development. DNA content analyses show that cell-autonomous PIDDosome loss causes an increase in nuclear and cellular CM ploidy. Increased ploidy does not affect cardiac structure nor function in early adulthood, but correlates with a modest reduction in cardiac performance in aged mice. PIDDosome-imposed polyploidy control commences at postnatal day 7 (P7), reaching a plateau by P14. PIDDosome activation requires ANKRD26, targeting PIDD1 to mother centrioles. Opposite to prior observations in liver development, the PIDDosome limits CM polyploidization in a p53-independent manner but reliant on induction of p21/Cdkn1a, a notion supported by nuclear RNA sequencing and genetic deletion experiments. Our results provide new insights how proliferation of polyploid CMs is restricted during postnatal heart development. - Source: PubMed
Publication date: 2026/01/12
Leone MKinz NEichin FObwegs DSladky V CBraun V ZHirschberger RRizzotto DEnglmaier LManzl CMoos KMergner JGiansanti PMartinez-Garcia NMarques M MJacotot E DEblahed LYousif RWright M KDawood DMaupome L SSavko CBoerries MSussman M AVillunger A