ZFP36L2 Antibody
- Known as:
- ZFP36L2 Antibody
- Catalog number:
- 40250
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- ZFP36L2 Antibody
Related genes to: ZFP36L2 Antibody
- Gene:
- ZFP36L2 NIH gene
- Name:
- ZFP36 ring finger protein like 2
- Previous symbol:
- BRF2
- Synonyms:
- ERF2, RNF162C, TIS11D
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-09
- Date modifiied:
- 2016-10-05
Related products to: ZFP36L2 Antibody
Related articles to: ZFP36L2 Antibody
- Rare coding genetic variants may exert large effects on risk of common disease, yet their contribution to disease architecture and their utility in gene prioritization remain limited by inadequate sample sizes. Here, we performed a massive-scale rare variant association study (RVAS), analyzing over 1.1 million sequenced participants among which 130,000 had atrial fibrillation (AF). Through a multi-mask burden testing approach, we identified 15 genes significantly associated with AF through rare large-effect variation. Integrative analyses revealed strong convergence between genes implicated by rare and common variation, and highlighted instances where RVAS data may aid in GWAS prioritization. Nevertheless, several RVAS genes were not among GWAS loci ( , , , ), or were not nominated through contemporary GWAS prioritization ( , ). Finally, we observed that ultra-rare protein-disrupting variants - concentrated in a small number of large-effect size genes - explained at least 2% of AF susceptibility across European and African ancestry groups. These findings refine the genetic architecture of AF, while highlighting the value and cost of RVAS for genomic discovery in common disease. - Source: PubMed
Publication date: 2026/05/04
Jurgens SeanEnzan NobuyukiDinsmore IanChoi Seung HoanLuo JonathanLipov AlexHartle CassandraWang XinMarston NicholasWeng Lu-ChenMelloni GiorgioChalazan BrandonGray MichaelPirruccello JamesDiaz AnnetteChaffin MarkOrnelas-Loredo AylinTang OwenDarbar FaisalKany ShinwanChen Yiningvon Falkenhausen AenneMorrison AlannaNatale AndreaTveit ArnljotGeelhoed BastiaanCade BrianWagoner David VanHaase DoreenSoliman Elsayed ZDavogustto GiovanniCalkins HughAnderson JefferyBrody JenniferBarnard JohnHokanson JohnSmith JonathanBis JoshuaYoung KendraJohnson LindaLong LeannRisch LorenzGula LorneKwee LydiaKühne MichaelPreuss MichaelGupta NamrataNafissi NavidSmith NicholasNilsson Petervan der Harst PimWells QuinnJudy RenaeSchnabel RenateJohnson ReneeSmit Roelof A JGabriel StaceyKnight StaceyFurukawa TetsushiMin Yuan-IYoneda ZacharyLaksman ZacharyAlonso AlvaroPsaty BruceAlbert ChristineArking DanRoden DanChasman DanielRader DanielConen DavidMcManus DavidFatkin DianeBoerwinkle EricMarcus GregoryChristophersen IngridSmith J GustavRoberts JasonRaffield LauraShoemaker M BenjaminCho MichaelCutler MichaelChung MinaOlesen MortenSinner MoritzSotoodehnia NonaKirchhof PaulusLoos Ruth J FNazarian SamanMohanty SanghamitraDamrauer ScottKaab StefanHeckbert SusanRedline SusanShah SvatiTanaka ToshihiroEbana YusukeLubitz StevenLunetta KathrynBenjamin EmeliaRienstra MichielFigtree GemmaDarbar DawoodBezzina ConnieRuff ChristianSabatine MarcMirshahi ToorajEllinor Patrick - - Source: PubMed
Publication date: 2026/04/20
Wang JiaxueSong JingyanChen WenLiang QihuiWu HaicuiGuan LuLian Fang - RNA-binding proteins, Zinc Finger Protein 36-Like 1 (ZFP36L1) and Zinc Finger Protein 36-Like 2 (ZFP36L2), post-transcriptionally regulate the expression of a large number of genes involved in various cellular processes. However, specific or redundant functions of ZFP36L1 and ZFP36L2 in liver homeostasis have never been explored. Here, we hypothesized that ZFP36L1 and ZFP36L2 are functionally redundant in the liver, and their combined deficiency would stabilize their direct mRNA targets, which would alter liver homeostasis. - Source: PubMed
Publication date: 2026/04/17
Kumar RahulBlackshear Perry JPatial SonikaSaini Yogesh - Zinc-finger protein 36 (Zfp36) family RNA-binding proteins, such as tristetraprolin (TTP/Zfp36), butyrate response factor (BRF)-1/Zfp36L1, and BRF-2/Zfp36L2, regulate the expression of cytokine/chemokine mRNA with AU-rich elements. In traumatic brain injury (TBI), reactive astrocytes produce various cytokines and chemokines that induce neuroinflammation. However, despite their importance in neuroinflammation, little is known about the regulation of cytokine and chemokine production by the Zfp36 family proteins in astrocytes. Endothelin-1 (ET-1), which promotes the conversion to reactive astrocytes, stimulates astrocytic cytokine and chemokine production. In the present study, we examined the effects of ET-1 on Zfp36 family protein expression in astrocytes and the roles of these proteins in cytokine/chemokine production. ET-1 (100 nM) increased the expression of TTP and BRF-1 in cultured astrocytes. In a mouse model of TBI, expression of TTP and BRF-1 increased, which was reduced by intracerebroventricular administration of BQ788, an ET antagonist. Immunohistochemical analyses showed that TTP and BRF-1 were present in reactive astrocytes. Knockdown of TTP by siRNA enhanced the production of ET-induced CCL2 and IL-6 in cultured astrocytes, while BRF-1 knockdown enhanced the CCL2, CXCL1, and CX3CL1 production. RNA immunoprecipitation/PCR analyses showed that ET-1 stimulated TTP binding to CCL2 and IL-6 mRNAs, and BRF-1 binding to CCL2, CXCL1, and CX3CL1 mRNAs. These results suggest that ET-1 stimulates the induction of TTP and BRF-1 in astrocytes and that the production of some astrocytic chemokine/cytokine is negatively regulated by the increments in TTP and BRF-1 production. - Source: PubMed
Publication date: 2026/04/02
Koyama YutakaNishiuma AinaTakahashi NagiIzumikawa EriHamada ChisatoIzumi YasuhikoHishinuma ShigeruMichinaga Shotaro - Type I interferons restrict HIV-1 replication by inducing antiviral genes, but the full spectrum of their effectors remains incompletely defined. Here we identify ZFP36L2, a nuclear RNA-binding protein, as an IFN-β-induced inhibitor of HIV-1 infection. Silencing of ZFP36L2 impairs IFN-β-mediated HIV-1 inhibition, whereas overexpression of ZFP36L2 suppresses viral replication. Notably, reconstitution of ZFP36L2 in CD4⁺ T cells from HIV-1-infected individuals reduces viral spread ex vivo, and ZFP36L2 transcript levels inversely correlate with plasma viral loads in vivo. Mechanistically, ZFP36L2 binds to the HIV-1 Rev protein and inhibits the nuclear export of Rev response element-containing viral transcripts, thereby blocking downstream viral protein expression. A Rev mutant lacking amino acids 109-116 fails to bind ZFP36L2 and exhibits resistance to ZFP36L2-mediated inhibition, underscoring the functional significance of this interaction. These findings establish ZFP36L2 as an IFN-β-induced antiviral factor that suppresses HIV-1 replication through Rev-dependent inhibition of viral RNA export. - Source: PubMed
Publication date: 2026/04/03
Pang HailinCui HualuYin XiaowanYang ZengwenShang HongLiang Guoxin