LIG3 Knock Down Cell Line (MTA Required priot to shipment) Knock Down
- Known as:
- LIG3 Knock Cell Line (MTA Required priot shipment) Knock Down
- Catalog number:
- 54999-001-01
- Product Quantity:
- 1 vial
- Category:
- -
- Supplier:
- Trevigen
- Gene target:
- LIG3 Knock Down Cell Line (MTA Required priot shipment)
Related genes to: LIG3 Knock Down Cell Line (MTA Required priot to shipment) Knock Down
- Gene:
- ABCB6 NIH gene
- Name:
- ATP binding cassette subfamily B member 6 (Langereis blood group)
- Previous symbol:
- -
- Synonyms:
- EST45597, umat, MTABC3
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2019-04-23
- Gene:
- ABCB10 NIH gene
- Name:
- ATP binding cassette subfamily B member 10
- Previous symbol:
- -
- Synonyms:
- EST20237, M-ABC2, MTABC2
- Chromosome:
- 1q42.13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2016-10-05
- Gene:
- C1orf35 NIH gene
- Name:
- chromosome 1 open reading frame 35
- Previous symbol:
- -
- Synonyms:
- MGC4174, MMTAG2
- Chromosome:
- 1q42.13
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-19
- Date modifiied:
- 2017-08-02
- Gene:
- CAMTA1-DT NIH gene
- Name:
- CAMTA1 divergent transcript
- Previous symbol:
- -
- Synonyms:
- lncCAMTA1
- Chromosome:
- 1p36.31
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2017-08-03
- Date modifiied:
- 2018-07-20
- Gene:
- DMAP1 NIH gene
- Name:
- DNA methyltransferase 1 associated protein 1
- Previous symbol:
- -
- Synonyms:
- DNMAP1, FLJ11543, KIAA1425, DNMTAP1, EAF2, MEAF2, SWC4
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-12
- Date modifiied:
- 2016-10-05
Related products to: LIG3 Knock Down Cell Line (MTA Required priot to shipment) Knock Down
Related articles to: LIG3 Knock Down Cell Line (MTA Required priot to shipment) Knock Down
- Metals are recognized as important factors related to breast cancer (BC) risk. Homologous recombination repair (HRR) genes might modify the toxicity of metals by influencing the distribution and metabolism of metal compounds. This study aims to investigate the modification effects of single nucleotide polymorphisms (SNPs) in HRR genes on the associations between urinary metals and BC risk. A total of 685 BC cases and 741 controls were recruited from October 2009 to December 2012. Twenty-one metals were analyzed in urine samples using inductively coupled plasma mass spectrometry (ICP-MS), and three SNPs (LIG3 rs1052536, RFC1 rs6829064, and RAD54L rs17102086) were genotyped. We identified significant interactions between four metals and two SNPs on the risk of BC. For LIG3 rs1052536 C/T variant, participants with CT/TT genotypes exposed to higher cobalt (Co) levels had higher BC risk compared to those with CC genotype (P = 0.048). For RAD54L rs17102086 T/C variant, participants with TT genotype who were exposed to higher levels of zinc (Zn), Co, arsenic (As), and strontium (Sr) had more pronounced BC risk than the CC/TC genotypes (all P < 0.05). This study showed compelling evidence for the interaction between genetic variants within the HRR system and urinary metals on BC risk. Our findings highlight the need to consider genetic makeup when evaluating the carcinogenic or protective potential of metals. - Source: PubMed
Publication date: 2024/05/08
Han ShushuLu MinjieZhang YixinLin YingLiu QiangXu LinRen Zefang - PARP1&2 enzymatic inhibitors (PARPi) are promising cancer treatments. But recently, their use has been hindered by unexplained severe anemia and treatment-related leukemia. In addition to enzymatic inhibition, PARPi also trap PARP1&2 at DNA lesions. Here, we report that unlike mice, which develop normally, mice expressing catalytically-inactive Parp2 (E534A, ) succumb to and -dependent erythropoietic failure , mirroring mice. While DNA damage mainly activates PARP1, we demonstrate that DNA replication activates PARP2 robustly. PARP2 is selectively recruited and activated by 5'-phosphorylated nicks (5'p-nicks) between Okazaki fragments, typically resolved by Lig1. Inactive PARP2, but not its active form or absence, impedes Lig1- and Lig3-mediated ligation, causing dose-dependent replication fork collapse, particularly harmful to erythroblasts with ultra-fast forks. This PARylation-dependent structural function of PARP2 at 5'p-nicks explains the detrimental effects of PARP2 inhibition on erythropoiesis, revealing the mechanism behind the PARPi-induced anemia and leukemia, especially those with TP53/CHK2 loss. - Source: PubMed
Publication date: 2024/03/14
Lin XiaohuiGupta DipikaVaitsiankova AlinaBhandari Seema KhattriLeung Kay Sze KarinaMenolfi DemisLee Brian JRussell Helen RGershik StevenGu WeiMcKinnon Peter JDantzer FrançoiseRothenberg EliTomkinson Alan EZha Shan - MNGIE (Mitochondrial Neurogastrointestinal Encephalomyopathy) is an ultra-rare autosomal recessive disorder that leads to mutations in the nuclear genes encoding thymidine phosphorylase. Symptoms include gastrointestinal dysmotility, cachexia, ptosis, external ophthalmoplegia, sensorimotor neuropathy and asymptomatic leukoencephalopathy. We describe the first case of MNGIE with meningoencephalitis that ultimately led to a familial diagnosis ending a diagnostic odyssey. We retrospectively reviewed the electronic medical records and sent whole exome sequencing for the index case and his family members. We report the variant c.877T>C p.(Cys293Arg) found in gene in all affected siblings showed typical clinical manifestations related to MNGIE. To the best of our knowledge, this is not described in the literature nor in the population databases dbSNP (Single Nucleotide Polymorphism Database) and gnomAD (Genome Aggregation Database). Additionally, it is located in a highly conserved residue and the bioinformatic analysis suggests it is most probably deleterious. Moreover, we estimated 550 number of cases of MNGIE (including 5 cases in this study) after performing an extensive search in the literature across 3 databases from 1983-2023. In addition, we identified 44 patients with MNGIE-like phenotype in genes other than . MNGIE-like phenotype affects , , and genes. - Source: PubMed
Publication date: 2024/03/27
Redha NoorAl-Sahlawi ZahraHasan HasanGhareeb SaraHumaidan Hani - This study focused on identifying potential key lncRNAs associated with gout under the mechanisms of copper death and iron death through ceRNA network analysis and Random Forest (RF) algorithm, which aimed to provide new insights into the molecular mechanisms of gout, and potential molecular targets for future therapeutic strategies of gout. Initially, we conducted an in-depth bioinformatics analysis of gout microarray chips to screen the key cuproptosis-related genes (CRGs) and key ferroptosis-related genes (FRGs). Using these data, we constructed a key ceRNA network for gout. Finally, key lncRNAs associated with gout were identified through the RF algorithm combined with ROC curves, and validated using the Comparative Toxicogenomics Database (CTD). We successfully identified NLRP3, LIPT1, and DBT as key CRGs associated with gout, and G6PD, PRKAA1, LIG3, PHF21A, KLF2, PGRMC1, JUN, PANX2, and AR as key FRGs associated with gout. The key ceRNA network identified four downregulated key lncRNAs (SEPSECS-AS1, LINC01054, REV3L-IT1, and ZNF883) along with three downregulated mRNAs (DBT, AR, and PRKAA1) based on the ceRNA theory. According to CTD validation inference scores and biological functions of target mRNAs, we identified a potential gout-associated lncRNA ZNF883/hsa-miR-539-5p/PRKAA1 regulatory axis. This study identified the key lncRNA ZNF883 in the context of copper death and iron death mechanisms related to gout for the first time through the application of ceRNA network analysis and the RF algorithm, thereby filling a research gap in this field and providing new insights into the molecular mechanisms of gout. We further found that lncRNA ZNF883 might function in gout patients by regulating PRKAA1, the mechanism of which was potentially related to uric acid reabsorption in the proximal renal tubules and inflammation regulation. The proposed lncRNA ZNF883/hsa-miR-539-5p/PRKAA1 regulatory axis might represent a potential RNA regulatory pathway for controlling the progression of gout disease. This discovery offered new molecular targets for the treatment of gout, and had significant implications for future therapeutic strategies in managing the gout. - Source: PubMed
Publication date: 2024/03/12
Shao Zi-ChenSun Wei-KangDeng Qin-QinCheng LingHuang XinHu Lie-KuiLi Hua-Nan - Nucleosomes, the basic structural units of chromatin, hinder recruitment and activity of various DNA repair proteins, necessitating modifications that enhance DNA accessibility. Poly(ADP-ribosyl)ation (PARylation) of proteins near damage sites is an essential initiation step in several DNA-repair pathways; however, its effects on nucleosome structural dynamics and organization are unclear. Using NMR, cryoelectron microscopy (cryo-EM), and biochemical assays, we show that PARylation enhances motions of the histone H3 tail and DNA, leaving the configuration of the core intact while also stimulating nuclease digestion and ligation of nicked nucleosomal DNA by LIG3. PARylation disrupted interactions between nucleosomes, preventing self-association. Addition of LIG3 and XRCC1 to PARylated nucleosomes generated condensates that selectively partition DNA repair-associated proteins in a PAR- and phosphorylation-dependent manner in vitro. Our results establish that PARylation influences nucleosomes across different length scales, extending from the atom-level motions of histone tails to the mesoscale formation of condensates with selective compositions. - Source: PubMed
Publication date: 2024/01/11
Nosella Michael LKim Tae HunHuang Shuya KateHarkness Robert WGoncalves MonicaPan AlisiaTereshchenko MariaVahidi SiavashRubinstein John LLee Hyun OForman-Kay Julie DKay Lewis E