Parp12 antibody - N-terminal region (OAAB03451)
- Known as:
- Parp12 (anti-) - N-terminal region (OAAB03451)
- Catalog number:
- oaab03451
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Parp12 antibody - N-terminal region (OAAB03451)
Related genes to: Parp12 antibody - N-terminal region (OAAB03451)
- Gene:
- PARP12 NIH gene
- Name:
- poly(ADP-ribose) polymerase family member 12
- Previous symbol:
- ZC3HDC1
- Synonyms:
- FLJ22693, PARP-12, ZC3H1
- Chromosome:
- 7q34
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-10
- Date modifiied:
- 2015-11-06
Related products to: Parp12 antibody - N-terminal region (OAAB03451)
Related articles to: Parp12 antibody - N-terminal region (OAAB03451)
- Targeting replication-associated DNA repair mechanisms, including the control of ADP-ribosylation by PARP1/2 and PARG, is a powerful therapeutic approach for cancer. However, the mechanisms by which PARG inhibition impacts DNA replication remain unclear. Here, we combine isolation of proteins on nascent DNA (iPOND) with quantitative proteomics and functional assays to investigate replication fork dynamics upon acute PARG inhibition. We find that FET family proteins (FUS, EWS, and TAF15) are recruited to replication forks in a PAR-dependent manner, forming condensates that slow fork progression and promote fork reversal. FET proteins control fork dynamics in response to some, but not all, replication stresses. FUS inactivation leads to unrestrained fork progression via RECQ1 and PRIMPOL, increased single-stranded DNA gaps, genome instability, and synthetic lethality with BRCA1 deficiency. These findings reveal that FET protein assemblies modulate replication stress responses, influencing genome stability and the cellular response to cancer therapeutics targeting PARylation pathways. - Source: PubMed
Publication date: 2026/06/30
Giansanti CelesteSchultz Jack CJackson JessicaVindigni AlessandroCortez David - PARP1/2 inhibitors (PARPi) are effective in cancer therapy due to their synthetic lethality in cells with defects in DNA double-strand break repair (DSBR). Here, we show that DSBR-proficient, naïve pluripotent mouse embryonic stem cells (mESC) exhibit high sensitivity towards PARP1/2 inhibition by talazoparib and olaparib. This sensitivity results from a two-tiered response of mESC to PARPi, starting with the activation of DNA stress signalling via ATM and followed by a p53-controlled, TET-TDG-dependent transcriptional response, including the de-repression of endogenous retroviral elements (ERVs). The resulting accumulation of double-stranded RNAs then elicits hallmarks of viral mimicry, marked by induction of type I interferon and necroptosis responses, alongside caspase activation. Accordingly, depletion of p53, TET, or TDG confers PARPi resistance in mESC. These findings highlight active DNA demethylation as a critical mediator of PARPi sensitivity in mESC and provide mechanistic insight into how DNA stress drives ERV expression in cells with accessible chromatin. - Source: PubMed
Xu JianmingSchwarz Simon DGunasekera KapilaSteinacher RolandKuśnierczyk AnnaHottiger Michael OSchär Primo - Breast cancer is the most frequently diagnosed malignant tumor and one of the leading causes of cancer deaths. Combination therapies, chemotherapy, and hormone therapy have indeed revolutionized the treatment of breast cancer, but they have not eliminated the occurrence of side effects. Among different anticancer strategies, plant-derived compounds appear to play a critical role in both prevention and therapy. They have been utilized in folk medicine for years, revealing anti-inflammatory, antimigraine, and anticancer properties. In particular, parthenolide derivatives have been shown to act as adjuvant agents in the treatment of various malignancies. Especially when provided with modifications that increase their bioavailability and stability. - Source: PubMed
Publication date: 2026/05/11
Nawrot JoannaTotoń EwaDziechciowska IgaBoruta AgnieszkaGołębiowska MałgorzataIdzik MałgorzataKaczmarek MariuszRubiś BłażejGornowicz-Porowska JustynaLisiak Natalia - Methotrexate (MTX)-induced liver injury (MTX-ILI) involves complex mechanisms that remain incompletely understood. This study investigated the role of NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis in MTX-ILI and explored the regulatory involvement of reactive oxygen species (ROS) and mitochondrial permeability transition pore (mPTP) opening. Wistar rats administered MTX and L02 cells exposed to MTX exhibited significant hepatocellular injury and pyroptotic features, as evidenced by elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and Caspase-1 activities; increased interleukin-1β (IL-1β) and interleukin-18 (IL-18) levels; and upregulation of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), gasdermin D (GSDMD), and its N-terminal fragment (GSDMD-N). These effects were attenuated by the NLRP3 inhibitor MCC950. In vitro, scavenging ROS with N-acetylcysteine (NAC) and inhibiting mPTP opening with ciclosporin A (CsA) markedly suppressed pyroptosis by alleviating mitochondrial dysfunction, reducing ROS accumulation, restoring mitochondrial membrane potential, and preserving mitochondrial ultrastructure. Label-free quantitative proteomics and protein-protein interaction analysis identified KNG1 and PARP12 as key proteins associated with ROS/mPTP-mediated pyroptosis, which were validated by Western blotting. Furthermore, Connectivity Map analysis predicted four potential therapeutic agents, including RS-127445, SB-218795, proadifen, and balicatib. Collectively, these findings demonstrate that MTX induces NLRP3-dependent pyroptosis through ROS accumulation and sustained mPTP opening. - Source: PubMed
Publication date: 2026/05/14
Cheng XuechunWu HaoZhuang XiupingYang BaohuiDing MingGao HongdaLi SijieLi QianWang Xin - The immunological composition of the microenvironment has shown relevance for diagnosis, prognosis, and therapy in solid tumors but remains underexplored in acute leukemias. We investigated the significance of the acute myeloid leukemia (AML) bone marrow microenvironment in predicting chemosensitivity and long-term remission in pediatric patients. We analyzed 32 non-promyelocytic pediatric AML patients at diagnosis using a NanoString PanCancer IO 360 assay, RNA sequencing, and deep-phenotype flow cytometry analyses. The findings were validated using the pediatric TARGET AML dataset. A short signature of three interferon (IFN)-related genes (, , and ) distinguished patients with chemosensitive disease and reduced minimal residual disease after induction chemotherapy. The signature stratified patients overall, and within the clinically defined "standard-risk" group, patients with high gene expression at diagnosis had significantly longer overall survival. The leukemia microenvironment associated with this signature showed enrichment of non-exhausted CD4 and CD8 T cytotoxic lymphocytes and expansion of CD8 T effector memory cells re-expressing CD45RA (TEMRA) in patients with a favorable prognosis. Our results show the importance of the bone marrow microenvironment in pediatric AML and provide tools for a refined stratification of "standard-risk" patients, lacking adequate risk-oriented therapies. They also offer a promising guide for tackling immune pathways and exploiting immune-targeted therapies. - Source: PubMed
Publication date: 2026/04/29
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