L3MBTL antibody - N-terminal region (ARP37760_P050)
- Known as:
- L3MBTL (anti-) - N-terminal region (ARP37760_P050)
- Catalog number:
- arp37760_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- L3MBTL antibody - N-terminal region (ARP37760_P050)
Related genes to: L3MBTL antibody - N-terminal region (ARP37760_P050)
- Gene:
- L3MBTL1 NIH gene
- Name:
- L3MBTL histone methyl-lysine binding protein 1
- Previous symbol:
- L3MBTL
- Synonyms:
- ZC2HC3, dJ138B7.3, DKFZp586P1522, KIAA0681
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-21
- Date modifiied:
- 2019-04-23
Related products to: L3MBTL antibody - N-terminal region (ARP37760_P050)
Related articles to: L3MBTL antibody - N-terminal region (ARP37760_P050)
- Chromatin is more than a simple genome packaging system but rather locally distinguished by histone post-translational modifications (PTMs) that can directly change nucleosome structure and/or be "read" by chromatin-associated proteins to mediate downstream events. An accurate understanding of histone PTM binding preference is vital to explain normal function and pathogenesis and has revealed multiple therapeutic opportunities. Such studies most often use histone peptides, though these cannot represent the full regulatory potential of nucleosome context. Here we apply a range of complementary and easily adoptable biochemical and genomic approaches to interrogate fully defined peptide and nucleosome targets with a diversity of mono- or multivalent chromatin readers. In the resulting data, nucleosome context consistently refined reader binding, and multivalent engagement was more often regulatory than simply additive. This included abrogating binding of the Polycomb group malignant brain tumor (MBT) protein L3MBTL1 to lysine methylated histone tails and confirmation that the CBX7 chromodomain and AT-hook-like motif (CD-ATL) tandem act as a functional unit to confer specificity for H3K27me3. These in vitro nucleosome preferences were confirmed by in vivo reader-CUT&RUN genomic mapping. Such data confirms that more representative chromatin substrates provide greater insight into biological mechanism and human disease. - Source: PubMed
Marunde Matthew RPopova Irina KHall Nathan WVaidya AnupBone James RBoone Brandon ABrown Peter JEzell Ryan JFirestone Tessa MFuchs Harrison AGibson ElisaGillespie Zachary BGloor Susan LHickman Allison RHoward Sarah AHusby Natalia LedoHsiung Victoria TJohnstone Andrea LKhan Laiba FKrajewski KrzysztofLee Alexander SMcAnarney Eileen TMaier Keith EMaryanski Danielle NMcCuiston Jamie LNoll Kelsey ENovitzky KatherinePatteson Emily FRodriguez Keli LSanchez Julio CSchachner Luis FSmith Catherine ESun LuTaylor Hailey FWatson RachelWillis Hannah EMusselman Catherine AVenters Bryan JCheek Marcus AMeiners Matthew JSun Zu-WenKelleher Neil LCowles Martis WWeinzapfel Ellen NKeogh Michael-ChristopherBurg Jonathan M - The lack of biomarkers to predict knee osteoarthritis (OA) progression is a key unmet need in the OA field. The objective of this study was to evaluate epigenetic changes in baseline peripheral blood cells of healthy individuals who subsequently developed radiographic knee OA (incident OA) as a preclinical biomarker. - Source: PubMed
Publication date: 2025/09/30
Brawner Cindy MirandaDyson GabriellaBarrett MontanaHanebutt NicholasSzymczak AleksanderMehta-D'souza PadmajaJeffries Matlock A - Cannabis vaping, particularly involving cannabidiol (CBD) and delta-9-tetrahydrocannabinol (THC), rapidly delivers highly concentrated cannabinoids to the brain, potentially affecting the hippocampus. This study examined differential expression of long noncoding RNAs (lncRNAs) and mRNAs in the hippocampus after acute exposure to vaporized CBD or THC. Male ICR mice were exposed to vaporized CBD or THC (50 mg, n = 5/group), and hippocampal tissues were collected at 1, 3, and 14 days post-exposure. Total RNA sequencing was conducted on day 1 samples, and selected transcripts were validated using qRT-PCR across multiple time points. CBD led to significant up- or downregulation of , , and at day 1. However, showed gradual recovery at days 3 and 14. In the THC group, , , and were significantly upregulated, while , , , and were significantly downregulated at day 1. Time-course analysis showed that expression returned to baseline by day 14, whereas remained persistently downregulated through days 3 and 14. In the CBD group, was upregulated, while and were downregulated at day 1; notably, showed a transient increase at day 3 before returning to baseline. In the THC group, and were upregulated, whereas , , and were downregulated, with most showing gradual recovery by day 14. Correlation analysis revealed that THC-responsive lncRNAs-including , , and -were strongly associated with downregulated mRNAs such as and . These findings highlight cannabinoid-specific hippocampal transcriptomic responses and suggest potential regulatory roles for lncRNA-mRNA interactions in cannabinoid-induced neural changes. - Source: PubMed
Publication date: 2025/07/23
Choi Mi RanKim JihunPark ChaeeunChang Seok HwanKim Han-NaJin Yeung BaeLee Sang-Rae - Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) is a fatal neurodegenerative disorder with only a limited number of risk loci identified. We report our comprehensive genome-wide association study as part of the International FTLD-TDP Whole-Genome Sequencing Consortium, including 985 patients and 3,153 controls compiled from 26 institutions/brain banks in North America, Europe and Australia, and meta-analysis with the Dementia-seq cohort. We confirm UNC13A as the strongest overall FTLD-TDP risk factor and identify TNIP1 as a novel FTLD-TDP risk factor. In subgroup analyzes, we further identify genome-wide significant loci specific to each of the three main FTLD-TDP pathological subtypes (A, B and C), as well as enrichment of risk loci in distinct tissues, brain regions, and neuronal subtypes, suggesting distinct disease aetiologies in each of the subtypes. Rare variant analysis confirmed TBK1 and identified C3AR1, SMG8, VIPR1, RBPJL, L3MBTL1 and ANO9, as novel subtype-specific FTLD-TDP risk genes, further highlighting the role of innate and adaptive immunity and notch signaling pathway in FTLD-TDP, with potential diagnostic and novel therapeutic implications. - Source: PubMed
Publication date: 2025/04/25
Pottier CyrilKüçükali FahriBaker MattBatzler AnthonyJenkins Gregory Dvan Blitterswijk MarkaVicente Cristina TDe Coster WouterWynants SarahVan de Walle PieterRoss Owen AMurray Melissa EFaura JúliaHaggarty Stephen Jvan Rooij Jeroen GjMol Merel OHsiung Ging-Yuek RGraff CarolineÖijerstedt LinnNeumann ManuelaAsmann YanMcDonnell Shannon KBaheti SaurabhJosephs Keith AWhitwell Jennifer LBieniek Kevin FForsberg LeahHeuer HilaryLago Argentina LarioGeier Ethan GYokoyama Jennifer SOddi Alexis PFlanagan MargaretMao QinwenHodges John RKwok John BDomoto-Reilly KimikoSynofzik MatthisWilke CarloOnyike ChiadiDickerson Bradford CEvers Bret MDugger Brittany NMunoz David GKeith JuliaZinman LorneRogaeva EkaterinaSuh EunRanGefen TamarGeula ChangizWeintraub SandraDiehl-Schmid JanineFarlow Martin REdbauer DieterWoodruff Bryan KCaselli Richard JDonker Kaat Laura LHuey Edward DReiman Eric MMead SimonKing AndrewRoeber SigrunNana Alissa LErtekin-Taner NiluferKnopman David SPetersen Ronald CPetrucelli LeonardUitti Ryan JWszolek Zbigniew KRamos Eliana MarisaGrinberg Lea TTempini Maria Luisa GornoRosen Howard JSpina SalvatorePiguet OlivierGrossman MurrayTrojanowski John QKeene C DirkJin Lee-WayPrudlo JohannesGeschwind Daniel HRissman Robert ACruchaga CarlosGhetti BernardinoHalliday Glenda MBeach Thomas GSerrano Geidy EArzberger ThomasHerms JochenBoxer Adam LHonig Lawrence SVonsattel Jean PLopez Oscar LKofler JuliaWhite Charles LGearing MarlaGlass JonathanRohrer Jonathan DIrwin David JLee Edward BVan Deerlin ViviannaCastellani RudolphMesulam Marsel MTartaglia Maria CFinger Elizabeth CTroakes ClaireAl-Sarraj SafaDalgard Clifton LMiller Bruce LSeelaar HarroGraff-Radford Neill RBoeve Bradley FMackenzie Ian Ravan Swieten John CSeeley William WSleegers KristelDickson Dennis WBiernacka Joanna MRademakers Rosa - Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (EGFR-TKI) approved for patients with EGFR T790M resistance mutations as first- or second-line treatment of EGFR-positive patients. Resistance to Osimertinib will inevitably develop, and the underlying mechanisms are largely unknown. In this study, we discovered that acquired resistance to Osimertinib is associated with abnormal DNA damage response (DDR) in lung adenocarcinoma cells. We discovered that the polycomb protein Lethal(3) Malignant Brain Tumor-Like Protein 1 (L3MBTL1) regulates chromatin structure, thereby contributing to DDR and Osimertinib resistance. EGFR oncogene inhibition reduced L3MBTL1 ubiquitination while stabilizing its expression in Osimertinib-resistant cells. L3MBTL1 reduction and treatment with Osimertinib significantly inhibited DDR and proliferation of Osimertinib-resistant lung cancer cells in vitro and in vivo. L3MBTL1 binds throughout the genome and plays an important role in EGFR-TKI resistance. It also competes with 53BP1 for H4K20Me2 and inhibits the development of drug resistance in Osimertinib-resistant lung cancer cells in vitro and in vivo. Our findings suggest that L3MBTL1 inhibition is a novel approach to overcoming EGFR-TKI-acquired resistance. - Source: PubMed
Publication date: 2024/09/04
Zhang ZiheLi YongwenShi RuifengJia ChaoyiXu SonglinZhu GuangshengCao PeijunHuang HuaLi XuanguangZhang HongbingLiu MinghuiChen ChenLiu HongyuKang ChunshengChen Jun