TIS11B / ZFP36L1 pSer92 antibody Ab
- Known as:
- TIS11B / ZFP36L1 pSer92 (anti-) Antibody
- Catalog number:
- 1488089
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- TIS11B / ZFP36L1 pSer92 antibody
Related genes to: TIS11B / ZFP36L1 pSer92 antibody Ab
- Gene:
- ZFP36L1 NIH gene
- Name:
- ZFP36 ring finger protein like 1
- Previous symbol:
- BRF1
- Synonyms:
- RNF162B, Berg36, ERF1, TIS11B, cMG1
- Chromosome:
- 14q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-09
- Date modifiied:
- 2016-06-30
Related products to: TIS11B / ZFP36L1 pSer92 antibody Ab
Related articles to: TIS11B / ZFP36L1 pSer92 antibody Ab
- Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and primary Sjögren's syndrome (pSS) frequently share overlapping clinical features, yet exhibit substantial intradisease heterogeneity in organ involvement and severity. This study aimed to define conserved molecular subtypes across these systemic autoimmune diseases (SADs) and delineate their transcriptional and epigenetic underpinnings. - Source: PubMed
Publication date: 2026/05/30
Fan YuSu MiaotongYu LijunChen ShaoqiZheng KediLin JianqunLin QishengZhang WeijinZheng ShaoyuZhou ZexuanZhang ShaohuiYuan XiaohanMatucci-Cerinic MarcoFurst Daniel EZhang GuohongWang Yukai - Innate lymphoid cells (ILCs) include T-bet-dependent NK and ILC1 cells, GATA-3-dependent ILC2 cells, and RORγt-dependent ILC3 cells. Their functional and developmental regulation at the posttranscriptional level remains elusive. The CCR4-NOT complex plays a central role in mRNA decay by mediating deadenylation. To explore the overall impact of mRNA decay on ILCs, we conditionally deleted Cnot3, an essential subunit of the CCR4-NOT complex. Loss of CNOT3 in ILC2 cells led to aberrant expression of T-bet and RORγt, accompanied by upregulation of type 1 and type 3 signature genes. Mechanistically, CNOT3 targeted the 3' untranslated regions of Tbx21 and Rorc mRNAs through interactions with Roquin and ZFP36L1, respectively. Elevated T-bet expression in CNOT3-deficient ILC2 cells suppressed GATA-3 levels, thereby impairing type 2 immune responses in models of airway allergy and helminth infection. Thus, our findings reveal that CNOT3 maintains ILC2 differentiation and function by restricting type 1 and type 3 transcriptional programs. - Source: PubMed
Publication date: 2026/05/12
Tatematsu MegumiTakasuga ShunsukeFuchimukai AkaneKimura YuumiIshii SatoshiTaniuchi IchiroIshiwata KenjiIkuta KoichiSexl VeronikaEberl GérardSawa ShinichiroKuba KeijiEbihara Takashi - Proliferative vitreoretinal diseases (PVDs) encompass severe ocular disorders such as proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR), and epiretinal membranes (ERM), characterized by the formation of fibrovascular membranes that often lead to retinal detachment and vision loss. A central mechanism driving these conditions is the epithelial-to-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells, orchestrated by a network of transcription factors (TFs). Among these, zinc finger E-box binding homeobox 1 (ZEB1) emerges as a pivotal regulator by repressing epithelial markers like E-cadherin and inducing mesenchymal markers such as N-cadherin and vimentin, thereby promoting cell migration and fibrotic membrane formation. nuclear factor of activated T cells 5 (NFAT5) contributes to this process by mediating osmotic stress responses and upregulating inflammatory cytokines, which further act upon EMT and fibrosis. activator protein 1 (AP-1) and hypoxia inducible factor 1 subunit alpha (HIF-1α) participate in driving inflammation, extracellular matrix (ECM) remodeling, and angiogenesis. While HIF-1α triggers vascular endothelial growth factor (VEGF) expression under hypoxic conditions, AP-1 modulates matrix metalloproteinases (MMPs) essential for ECM degradation and remodeling. Additional TFs, including Kruppel-like factor 4 (KLF4) and microphthalmia-associated transcription factor (MITF), are vital in maintaining RPE cell identity. Their downregulation under pathological conditions disrupts epithelial integrity and predisposes cells to undergo EMT. Moreover, β-catenin, through its role in the wingless-related integration site (Wnt) signaling pathway, reinforces EMT and ECM remodeling, further enhancing fibrotic progression. Adipocyte enhancer-binding protein 1 (AEBP1) and ZFP36 ring finger protein like 1 (ZFP36L1) also regulate inflammatory responses and ECM dynamics, providing novel post-transcriptional targets for therapeutic intervention. Overall, the synergistic interactions among these TFs create complex feedback loops that amplify pathological changes in PVDs. Targeting these molecular pathways offers promising avenues for developing multi-targeted therapies aimed at saving vision-threatening disease while reducing invasive surgical interventions. - Source: PubMed
Publication date: 2026/05/08
Duveau ClémentRaiss El Harrak YosraDatlibagi AzinePerret JasonWillermain FrançoisDelporte ChristineMotulsky Elie - Microglia play an important role in ischemic stroke (IS). However, the molecular regulatory mechanisms underlying microglial ferroptosis in IS remain incompletely understood. In this study, blood samples were collected from 20 IS patients and 15 healthy volunteers. Microglia BV-2 subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) and mice undergoing middle cerebral artery occlusion-reperfusion (MCAO/R) surgery were used to establish IS models. Our results revealed that in blood samples from IS patients and in OGD/R-treated BV-2 cells, ZFP36 ring finger protein like 1 (ZFP36L1) and Acyl-CoA synthetase long chain family member 1 (ACSL1) expression was increased, while the fat mass and obesity-associated (FTO) protein expression was decreased. ACSL1 silencing attenuated ferroptosis and inflammation in OGD/R-treated microglia, as evidenced by decreased levels of malondialdehyde, Fe, lipid peroxidation, inflammatory factors, along with an increased Glutathione/Glutathione disulfide ratio. Additionally, ZFP36L1 silencing suppressed the OGD/R-induced promotion of ferroptosis and inflammation in microglia and alleviated cerebral ischemic injury in MCAO/R mice, whereas ACSL1 overexpression reversed these alterations caused by ZFP36L1 silencing. Mechanistically, ZFP36L1 decreased FTO messenger RNA (mRNA) stability and reduced FTO expression. FTO overexpression reduced ACSL1 N6-methyladenosine (m6A) modification and ACSL1 expression. In conclusion, ZFP36L1 increased ACSL1 m6A modification and ACSL1 expression to promote microglial ferroptosis, neuroinflammatory response, and cerebral ischemic injury in IS by reducing FTO mRNA stability. - Source: PubMed
Publication date: 2026/04/29
Song Ai-XiaJin Han-XuSun Yuan-XinKou Wen-HuiNiu Xiao-NingWang Huan-HuanZhong Ting-TingGu Ping - RNA-binding proteins (RBPs) and ferroptosis have been demonstrated to play important roles in the progression of chronic rhinosinusitis (CRS). However, the regulatory mechanisms underlying the interaction between RBPs and ferroptosis in CRS, particularly regarding mitochondrial metabolism, remain elusive. - Source: PubMed
Xiong JiayiZhang ShihanLi ChunhuaAi YufengLiu XinruLiu YuxiangLiu Hongbing