Affinage

ZFP36L1

mRNA decay activator protein ZFP36L1 · UniProt Q07352

Round 2 corrected
Length
338 aa
Mass
36.3 kDa
Annotated
2026-04-28
130 papers in source corpus 29 papers cited in narrative 29 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ZFP36L1 is a tandem CCCH zinc-finger RNA-binding protein that recognizes AU-rich elements (AREs) in the 3′-UTRs of target mRNAs and promotes their deadenylation and degradation by recruiting the CCR4-NOT deadenylase complex, decapping enzymes, and exonucleases, thereby delivering ARE-containing transcripts to processing bodies (PMID:12198173, PMID:15687258, PMID:25106868, PMID:17369404). Its mRNA-destabilizing activity is reversibly inactivated by PKB/Akt phosphorylation at S92 and S203, which induces 14-3-3 binding and protects ZFP36L1 from proteasomal degradation, and by MK2 phosphorylation, while RSK-mediated phosphorylation dissociates the CCR4-NOT complex to stabilize target mRNAs (PMID:17030608, PMID:18326031, PMID:25106868). Through post-transcriptional control of functionally diverse ARE-containing mRNAs—including VEGF, HIF1A, CCND1, Nanog, Cyp7a1, SOX2, INSM1, Stat5b, GRK2, and BCL2—ZFP36L1 regulates lymphocyte quiescence, erythroid differentiation, bile acid metabolism, neuroendocrine cell plasticity, satellite cell maintenance, and antibody-secreting cell homing (PMID:27102483, PMID:20702587, PMID:28891815, PMID:36008402, PMID:30526691, PMID:33306108). Conditional knockout studies demonstrate that ZFP36L1 acts redundantly with ZFP36L2 in B-cell quiescence and muscle satellite cell biology, while uniquely controlling hepatic Cyp7a1 mRNA turnover to regulate bile acid homeostasis and protect against diet-induced obesity (PMID:27102483, PMID:30526691, PMID:28891815).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1996 Low

    Initial characterization established ZFP36L1 as an immediate-early gene induced by mitogens and calcium signaling, but its molecular function was unknown.

    Evidence Northern blot in mitogen-stimulated epithelial cells and antisense knockdown in B cells showing partial apoptosis inhibition

    PMID:1628738 PMID:8898945

    Open questions at the time
    • No molecular function identified beyond expression induction
    • Antisense knockdown apoptosis result not independently confirmed
    • No direct target mRNAs identified
  2. 2002 High

    A genetic rescue screen established ZFP36L1 as an essential ARE-mRNA decay factor, resolving its molecular function as an RNA-binding protein that accelerates mRNA turnover through its zinc-finger domains.

    Evidence Retroviral cDNA rescue of ARE-decay-deficient slowC cells carrying biallelic ZFP36L1 frameshift mutations, validated by siRNA and zinc-finger mutagenesis

    PMID:12198173

    Open questions at the time
    • Mechanism of decay enzyme recruitment unknown
    • Identity of endogenous mRNA targets unresolved
  3. 2004 High

    The mechanism by which ZFP36L1 couples ARE recognition to mRNA destruction was elucidated: it contains activation domains that recruit deadenylases, decapping enzymes, and exonucleases, and its first physiological target—VEGF mRNA—was identified.

    Evidence Co-IP of decay enzymes with ZFP36L1, tethered decay assays, RNP-IP confirming VEGF mRNA binding, and half-life measurements in primary adrenocortical cells

    PMID:14976220 PMID:15467755 PMID:15687258

    Open questions at the time
    • Structural basis for decay enzyme recruitment unknown
    • Full repertoire of endogenous targets not defined
  4. 2004 High

    Discovery that PKB/Akt phosphorylates ZFP36L1 at S92 to inhibit its decay activity without blocking ARE binding revealed the first signaling mechanism controlling this protein, with 14-3-3 sequestration as the inactivation mode.

    Evidence In vitro kinase assay, reconstituted decay assay with phospho-mimetic mutants, co-IP with 14-3-3

    PMID:15538381

    Open questions at the time
    • Contribution of additional phosphosites unknown
    • In vivo relevance of PKB regulation not tested
  5. 2006 High

    The phosphoregulation model was refined: cooperative PKB phosphorylation at both S92 and S203 is required for 14-3-3 binding and ZFP36L1 protein stabilization, revealing that ZFP36L1 is a labile protein whose abundance and activity are co-regulated by the same phosphorylation events.

    Evidence Double S92A/S203A mutagenesis, proteasome inhibitor rescue, PKBα knockout cells

    PMID:17030608

    Open questions at the time
    • Ubiquitin ligase responsible for ZFP36L1 degradation not identified
    • Relationship between protein turnover and functional output in vivo unclear
  6. 2007 High

    ZFP36L1 was shown to deliver ARE-mRNAs to processing bodies for degradation, establishing its role in subcellular compartmentalization of mRNA decay.

    Evidence siRNA depletion, fluorescent mRNA tracking, and tethering assays in human cells

    PMID:17369404

    Open questions at the time
    • Whether P-body localization is required for or merely accompanies decay not resolved
    • Relative contribution of cytoplasmic vs. P-body decay unclear
  7. 2008 High

    MK2 was identified as a second kinase inactivating ZFP36L1 at overlapping sites (S54, S92, S203), acting downstream of p38 MAPK stress signaling and inhibiting decay at a step beyond RNA binding and enzyme recruitment.

    Evidence In vitro kinase assays with ZFP36L1 fragments, active MK2 co-expression, ARE-decay functional assays

    PMID:18326031

    Open questions at the time
    • Exact post-recruitment step blocked by MK2 phosphorylation unknown
    • Relative physiological importance of MK2 vs. PKB phosphorylation undefined
  8. 2014 High

    The CCR4-NOT deadenylase complex was identified as the specific effector recruited by ZFP36L1's C-terminus, and RSK (downstream of ERK) was shown to phosphorylate this region to dissociate CCR4-NOT and stabilize target mRNAs such as LDLR, completing the picture of three kinase inputs converging on ZFP36L1.

    Evidence Proteomic 3′-UTR pull-down, CCR4-NOT co-IP, in vitro RSK phosphorylation, antisense oligonucleotide validation

    PMID:25106868

    Open questions at the time
    • Structural basis of CCR4-NOT interaction and its phosphorylation-dependent dissociation not resolved
    • Relative contribution of deadenylation vs. other decay routes for individual targets unknown
  9. 2014 Medium

    ZFP36L1's target repertoire was expanded to include Nanog mRNA in embryonic stem cells, positioning it as an effector of FGF/ERK signaling that attenuates pluripotency and biases mesendoderm differentiation.

    Evidence Conditional overexpression in mESCs, Nanog mRNA half-life measurement, ERK pathway epistasis

    PMID:24733888

    Open questions at the time
    • Full ZFP36L1 target set in ESCs not defined
    • In vivo embryonic phenotype of Zfp36l1 loss not reported in this context
  10. 2016 High

    Conditional double knockout of Zfp36l1 and Zfp36l2 in B cells revealed that these proteins enforce quiescence during lymphocyte development by suppressing a post-transcriptional regulon of cell-cycle-promoting mRNAs, establishing a physiological role in adaptive immunity.

    Evidence Conditional double KO mice, RNA-seq, BrdU cell-cycle analysis, V(D)J recombination assays

    PMID:27102483

    Open questions at the time
    • Individual contributions of ZFP36L1 vs. ZFP36L2 to the quiescence regulon not separated
    • Identity of critical individual target mRNAs within the regulon not fully resolved
  11. 2017 High

    ZFP36L1 was established as a metabolic regulator downstream of FXR: it destabilizes Cyp7a1 mRNA to control bile acid synthesis, and hepatic deletion protects against diet-induced obesity, linking mRNA decay to systemic metabolic homeostasis.

    Evidence Conditional hepatic Zfp36l1 KO, AAV overexpression, Cyp7a1 mRNA half-life, bile acid quantification, diet-induced obesity model

    PMID:28891815

    Open questions at the time
    • Whether additional hepatic ZFP36L1 targets contribute to the metabolic phenotype not defined
    • Human relevance of the Cyp7a1-bile acid axis regulation by ZFP36L1 not tested
  12. 2018 High

    Functional redundancy between ZFP36L1 and ZFP36L2 was demonstrated in muscle satellite cells, where double but not single knockout caused satellite cell depletion and impaired regeneration, extending the quiescence-enforcement paradigm beyond lymphocytes to stem cell biology.

    Evidence Single and double conditional KO in Pax7+ satellite cells, cardiotoxin injury regeneration model

    PMID:30526691

    Open questions at the time
    • Direct mRNA targets in satellite cells not identified
    • Mechanism of satellite cell loss (exhaustion vs. differentiation vs. death) not resolved
  13. 2019 High

    ZFP36L1's tumor-suppressor function was mechanistically defined through identification of HIF1A, CCND1, and E2F1 as direct targets, linking ARE-mediated decay to suppression of hypoxic signaling and cell-cycle progression, while systematic RNA pull-down identified over 1,400 potential target mRNAs.

    Evidence RNA pull-down with WT vs. zinc-finger mutant ZFP36L1, transcriptome-wide sequencing, RNA-EMSA, reporter assays, in vivo xenograft

    PMID:31551365

    Open questions at the time
    • Fraction of 1,410 candidate targets that are functionally relevant unknown
    • Whether tumor-suppressor activity is context-dependent across cancer types not established
  14. 2021 High

    ZFP36L1 was found to direct antibody-secreting cell trafficking to bone marrow by regulating GRK2 and integrin α4/β1 mRNA levels, revealing a role in immune cell migration distinct from its quiescence function.

    Evidence Conditional KO mice, flow cytometry of ASC distribution, identification of GRK2 and integrin mRNAs as direct targets

    PMID:33306108

    Open questions at the time
    • Whether ZFP36L1 controls homing of other immune cell types unknown
    • Mechanism discriminating which targets are regulated in ASCs vs. other cell types unclear
  15. 2022 High

    ZFP36L1 was identified as a master regulator of neuroendocrine plasticity in SCLC: it destabilizes SOX2 and INSM1 mRNAs, and its epigenetic silencing by LSD1 is required for maintenance of the neuroendocrine phenotype, explaining LSD1 inhibitor sensitivity.

    Evidence Genome-wide CRISPR screen, RNA-IP for SOX2/INSM1, mRNA stability assays, LSD1 ChIP

    PMID:36008402

    Open questions at the time
    • Whether ZFP36L1 controls neuroendocrine plasticity in other tumor types unknown
    • Full set of ZFP36L1 targets mediating phenotypic switching not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • The structural basis for ZFP36L1's selective recruitment of the CCR4-NOT complex and how phosphorylation at distinct sites differentially modulates deadenylase association, P-body delivery, and proteasomal turnover remains unresolved; the rules governing target selectivity among the >1,400 candidate ARE-mRNAs in different cell types are also undefined.
  • No crystal or cryo-EM structure of ZFP36L1 in complex with CCR4-NOT or ARE RNA
  • Target selectivity rules across cell types not defined
  • In vivo contribution of individual phosphorylation sites (S54, S92, S203) not dissected by knock-in

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 7 GO:0140098 catalytic activity, acting on RNA 4 GO:0098772 molecular function regulator activity 2
Localization
GO:0005829 cytosol 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-8953854 Metabolism of RNA 5 R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 3 R-HSA-1640170 Cell Cycle 2 R-HSA-168256 Immune System 2 R-HSA-1430728 Metabolism 1
Partners
CNOT1DCP1APARNXRN1YWHAB

Evidence

Reading pass · 29 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 ZFP36L1 (BRF1) was functionally identified as an essential regulator of AU-rich element (ARE)-dependent mRNA decay. Genetic rescue of a mutant cell line (slowC) deficient in ARE-mRNA degradation by retroviral cDNA library screening identified BRF1 as the causative gene; slowC carried frame-shift mutations in both BRF1 alleles. siRNA knockdown and transfection experiments confirmed that BRF1 accelerates ARE-mRNA decay and that its zinc-finger domains are required for both ARE binding and mRNA destabilization activity. Retroviral cDNA library functional rescue screen, flow cytometry of GFP-ARE reporter, siRNA knockdown, zinc-finger mutagenesis The EMBO journal High 12198173
2004 ZFP36L1 (BRF1) mRNA-destabilizing activity is regulated by protein kinase B (PKB/Akt), which phosphorylates BRF1 at serine 92 (S92). Phosphorylation by PKB impairs BRF1's in vitro ARE-mRNA decay activity without affecting ARE binding, but induces complex formation with the scaffold protein 14-3-3, sequestering BRF1 and stabilizing ARE-containing transcripts. In vitro mRNA decay assay with recombinant BRF1, in vitro kinase assay, co-immunoprecipitation with 14-3-3, site-directed mutagenesis (S92A) The EMBO journal High 15538381
2004 ZFP36L1 (TIS11b) binds to AU-rich elements in the 3'-UTR of VEGF mRNA and destabilizes it, reducing VEGF mRNA half-life from ~130 to ~60 min. A 75 bp domain containing two consensus AU-rich motifs was identified as the binding and destabilization target. RNP immunoprecipitation confirmed the interaction in live cells, and siRNA knockdown of TIS11b elevated VEGF mRNA levels in primary adrenocortical cells. mRNA half-life measurements, RNP immunoprecipitation, deletion mapping of 3'-UTR, siRNA knockdown Oncogene High 15467755
2004 ZFP36L1 (BRF1) and TTP each contain two activation domains that recruit mRNA decay enzymes (deadenylases, decapping enzymes, and exonucleases) involved in deadenylation, decapping, and 3'-to-5' and 5'-to-3' exonucleolytic decay. BRF-1's N-terminal activation domain functions as a binding platform for mRNA decay machinery, linking ARE-containing mRNAs to the decay apparatus. Co-immunoprecipitation of decay enzymes with BRF-1, tethered mRNA decay assays with heterologous RNA-binding domain fusions, dominant-negative overexpression Genes & development High 15687258
2004 siRNA-mediated knockdown of BRF1 (ZFP36L1) stabilized ARE-reporter mRNA and increased fluorescence of a GFP-ARE reporter in HT1080 cells, confirming its endogenous role as an ARE-mRNA destabilizer. Selective knockdown of p40AUF1/p45AUF1 but not BRF1 stabilized GM-CSF mRNA, demonstrating that BRF1 and AUF1 regulate overlapping but distinct ARE-mRNA subsets. siRNA knockdown, fluorescent ARE-reporter assay, GM-CSF mRNA stability measurement Nucleic acids research Medium 14976220
2006 BRF1 (ZFP36L1) protein stability and mRNA decay activity are co-regulated by PKB/Akt phosphorylation at two cooperative sites, S92 and S203. Phosphorylation at both sites is required for 14-3-3 binding, BRF1 protein stabilization (preventing proteasomal degradation), and inactivation of ARE-mRNA decay. Alanine mutations at both sites uncoupled BRF1 from PKB regulation, causing constitutive mRNA decay. BRF1 is labile (half-life <3 h) and stabilized by phosphorylation-dependent 14-3-3 binding. In vitro kinase assay, site-directed mutagenesis (S92A/S203A), proteasome inhibitor experiments, cell fractionation, PKBα knockout cells Molecular and cellular biology High 17030608
2007 ZFP36L1 (BRF-1) and TTP deliver ARE-mRNAs to processing bodies (PBs) in human cells. Depletion of endogenous TTP and BRF proteins impaired localization of ARE-reporter mRNAs to PBs. BRF-1 can tether mRNAs to PBs and TTP can nucleate PB formation on untranslated mRNAs. ARE-mRNA PB localization requires the TTP/BRF-1 N- and C-terminal domains and occurs downstream of mRNA polysome release. siRNA depletion, fluorescent reporter mRNA tracking, dominant-negative overexpression, tethering assays Genes & development High 17369404
2008 ZFP36L1 (BRF1) is phosphorylated by MAPK-activated protein kinase 2 (MK2) at four sites including S54, S92, and S203, which inhibits its ARE-mRNA decay activity. This inhibition does not alter BRF1's ability to bind AREs or associate with mRNA decay enzymes, suggesting MK2 targets a step downstream of RNA binding and decay enzyme recruitment. In vitro kinase assay with BRF1 fragments, co-expression of active MK2, ARE-mRNA decay assays, mutagenesis of phosphorylation sites RNA High 18326031
2009 ZFP36L1 (TIS11b) regulates steroidogenic acute regulatory protein (StAR) mRNA stability through direct binding to UAUUUAUU AU-rich repeats in the extended 3'-UTR of the 3.5-kb StAR transcript. Cotransfection of TIS11b selectively decreased cytomegalovirus-driven Star mRNA and luciferase-Star 3'-UTR reporters. siRNA knockdown of TIS11b specifically enhanced 3.5-kb Star mRNA induction and halved STAR protein induction, demonstrating coupling of mRNA decay to cholesterol metabolism in steroidogenic cells. Direct RNA complex formation assay, luciferase-3'UTR reporter assay, siRNA knockdown, ARE mutagenesis, cotransfection Molecular endocrinology High 19179481
2009 ZFP36L1 (TIS11b/ZFP36L1) expression is regulated by VHL tumor suppressor protein in renal cancer cells. In normoxia, VHL overexpression increased hsa-miR-29b levels, which decreased TIS11B protein by post-transcriptional regulation. In hypoxia, VHL overexpression increased TIS11B mRNA stability and protein levels, which in turn downregulated VEGF mRNA. Silencing TIS11B reversed VHL-mediated VEGF downregulation in hypoxia. miRNA expression analysis, TIS11B knockdown with siRNA, VEGF mRNA and protein quantification, TIS11B mRNA stability assay The Journal of biological chemistry Medium 19801654
2010 ZFP36L1 negatively regulates erythroid differentiation of CD34+ hematopoietic stem cells by directly binding the 3'-UTR of Stat5b mRNA to trigger its degradation, thereby reducing STAT5B protein levels. ZFP36L1 overexpression dramatically decreased erythroid colony formation in human hematopoietic progenitors, and this effect was confirmed by Stat5b siRNA knockdown. Co-overexpression of ZFP36L1 and ZFP36 had a cumulative effect on Stat5b downregulation. 3'-UTR RNA binding assay, overexpression in CD34+ cells, erythroid colony assay, siRNA knockdown of Stat5b, co-overexpression experiments Molecular biology of the cell Medium 20702587
2010 Cell-penetrating fusion proteins of ZFP36L1 (R9-ZFP36L1, TAT-ZFP36L1) were efficiently internalized into living cells and decreased endogenous VEGF mRNA half-life and VEGF protein levels. Intratumoral injection of R9-ZFP36L1 in Lewis Lung Carcinoma mouse models significantly reduced tumor growth and decreased expression of multiple angiogenic and inflammatory cytokines (VEGF, FGF-a, TNFα, IL-1α, IL-6), with concomitant reduction in tumor vascularization. Protein transduction domain fusion constructs, in vitro mRNA decay assays, intratumoral injection in mouse tumor model, cytokine quantification Oncogene Medium 20802528
2010 ZFP36L1 (ZFP36L1) is induced by growth factors and cytokines in keratinocytes (EGF, FGF, serum, etc.) and by scratch wounding. siRNA-mediated knockdown of ZFP36L1 in HaCaT keratinocytes prolonged elevated VEGF mRNA levels following EGF stimulation, consistent with ZFP36L1 destabilizing VEGF mRNA in the wound healing context. siRNA knockdown, VEGF mRNA quantification, scratch wound assay Growth factors Low 20166898
2014 ZFP36L1 (Brf1) operates downstream of FGF/ERK MAP kinase signaling in mouse embryonic stem cells (mESCs) to regulate pluripotency by destabilizing target mRNAs including Nanog. FGF/ERK signaling upregulates Brf1, which disrupts core pluripotency gene expression and attenuates mESC self-renewal. Brf1 overexpression preferentially regulates mesendoderm commitment during differentiation, accelerating primitive streak marker expression. Conditional Brf1 overexpression in mESCs, mRNA stability assays (Nanog half-life), ERK pathway manipulation, differentiation assays with lineage markers Proceedings of the National Academy of Sciences Medium 24733888
2014 ZFP36L1 and ZFP36L2 bind to the 3'-UTR of LDLR mRNA and recruit the CCR4-NOT deadenylase complex, destabilizing LDLR mRNA. The C-terminal regions of ZFP36L1 and ZFP36L2 are directly phosphorylated by p90 ribosomal S6 kinase (RSK, downstream of ERK), causing dissociation of the CCR4-NOT complex and stabilization of LDLR mRNA. Antisense oligonucleotides targeting the ZFP36L1/L2 binding sites on LDLR mRNA upregulated LDLR mRNA and protein. Proteomic identification of 3'-UTR binding proteins (pull-down MS), CCR4-NOT co-immunoprecipitation, in vitro phosphorylation by RSK, antisense oligonucleotide experiments Nucleic acids research High 25106868
2014 ZFP36L1 (ZFP36L1) binds the BCL2 3'-UTR AU-rich element and mediates BCL2 mRNA degradation in malignant B cells. RNA electrophoretic mobility shift assay (REMSA) showed direct ZFP36L1-BCL2 ARE interaction. ZFP36L1 knockdown in BCL1, ACHN, and Ramos cells increased BCL2 mRNA levels. Luciferase reporter assays showed wild-type but not zinc-finger mutant ZFP36L1 downregulated BCL2 ARE-containing constructs; deletion of the ARE core abrogated this effect. RNA EMSA, siRNA/shRNA knockdown in multiple cell lines, 3'UTR luciferase reporter assay, zinc-finger domain mutagenesis PloS one Medium 25014217
2015 In LPS-stimulated RAW264.7 macrophages, ZFP36L1 protein is hyperphosphorylated, which promotes complex formation with 14-3-3 adapter protein and decreases interaction with the CCR4-NOT deadenylase subunit Caf1a. Knockdown of Zfp36l1 increased basal Mkp-1 mRNA levels by prolonging its half-life, and this elevated MKP-1 inhibited p38 MAPK activation during LPS stimulation, consequently downregulating TNFα and TTP expression. siRNA knockdown, mRNA half-life assay, co-immunoprecipitation (14-3-3 and Caf1a), phosphorylation analysis Journal of inflammation Medium 26180518
2016 ZFP36L1 and ZFP36L2 are critical for maintaining quiescence in developing B lymphocytes before pre-BCR expression and for reestablishing quiescence after pre-BCR-induced expansion. These proteins suppress a posttranscriptional regulon of mRNAs whose protein products cooperatively promote S-phase entry, thus promoting VDJ recombination and selection of cells expressing immunoglobulin-μ at the pre-BCR checkpoint. Conditional knockout mice (Zfp36l1/l2 double KO in B cells), RNA-seq, BrdU incorporation cell-cycle analysis, V(D)J recombination assays Science High 27102483
2017 ZFP36L1 is an FXR target gene that post-transcriptionally regulates bile acid metabolism by destabilizing Cyp7a1 mRNA. Gain-of-function and loss-of-function of ZFP36L1 reciprocally regulated Cyp7a1 mRNA and bile acid levels in vivo. Mice with hepatic ZFP36L1 deletion were protected from diet-induced obesity and hepatosteatosis due to impaired lipid absorption linked to altered bile acid metabolism. Conditional hepatic Zfp36l1 KO mice, adeno-associated virus overexpression, Cyp7a1 mRNA half-life assay, bile acid quantification, diet-induced obesity model The Journal of clinical investigation High 28891815
2018 ZFP36L1 and ZFP36L2 inhibit cell proliferation and arrest the cell cycle at G1 phase in a cyclin D-dependent and p53-independent manner. Forced expression of ZFP36L1 inhibited cyclin D expression and cell proliferation in p53-null and p53-mutant colorectal cancer cell lines. Zinc-finger domain mutation abolished these antiproliferative effects, confirming that RNA-binding activity through the tandem zinc-finger domain is required. Inducible overexpression, siRNA knockdown, cell cycle analysis (flow cytometry), cyclin D mRNA/protein measurements, zinc-finger domain mutagenesis in three cell lines including p53 KO Scientific reports Medium 29426877
2019 ZFP36L1 directly regulates OA pathogenesis in chondrocytes by destabilizing mRNAs of two HSP70 family members (HSPA1A and related members). ZFP36L1 is specifically upregulated in OA chondrocytes. Genetic ablation or silencing of Zfp36l1 abrogated experimental OA in mice, and this was associated with increased HSP70 expression. Overexpression of HSPA1A in joint tissue protected against OA by inhibiting chondrocyte apoptosis. Adenovirus-mediated overexpression/knockdown, genetic KO mouse OA model (intraarticular injection), identification of HSP70 as direct mRNA targets, HSPA1A overexpression rescue experiment Nature communications High 30622281
2019 ZFP36L1 functions as a tumor suppressor by binding to ARE sequences in the 3'-UTRs of HIF1A, CCND1, and E2F1 mRNAs for degradation, suppressing hypoxic signaling and cell-cycle progression. Wild-type but not zinc-finger-mutant ZFP36L1 bound HIF1A 3'-UTR in dual luciferase reporter assays and RNA-EMSA, mediating HIF1A mRNA degradation. Systematic RNA pull-down with WT vs. mutant ZFP36L1 and whole-transcriptome sequencing identified 1,410 potential direct targets. RNA pull-down with WT vs. zinc-finger mutant ZFP36L1, transcriptome sequencing, dual luciferase reporter assay, RNA-EMSA, forced expression and silencing in bladder cancer cells in vitro and in vivo Cancer research High 31551365
2020 miR-93-3p promotes keratinocyte proliferation and migration during skin wound healing by directly targeting ZFP36L1, reducing its expression. ZFP36L1 silencing mirrored miR-93-3p overexpression effects on proliferation and migration. ZFP36L1 in turn targets ZFX mRNA for degradation; ZFX overexpression promoted proliferation and migration, placing ZFP36L1 upstream of ZFX in keratinocyte wound-healing signaling. In vivo mouse wound model, miRNA overexpression/inhibition, siRNA knockdown, luciferase 3'UTR reporter assay for miR-93-3p→ZFP36L1 and ZFP36L1→ZFX interactions Molecular therapy. Nucleic acids Medium 33473330
2021 ZFP36L1 facilitates antibody-secreting cell (ASC) homing to the bone marrow by directly regulating the mRNA abundance of G protein-coupled receptor kinase 2 (GRK2) and the integrin chains α4 and β1. Loss of ZFP36L1 caused ASC accumulation in spleen and liver with reduced bone marrow homing. Differential effects on early vs. late ASCs correlated with the expression of CXCR4 and integrins α4/β1 regulated by ZFP36L1. Zfp36l1 conditional KO mice, flow cytometry of ASC localization, identification of GRK2/integrin α4/β1 as direct ZFP36L1 mRNA targets, CXCR4 expression analysis The Journal of experimental medicine High 33306108
2022 ZFP36L1 controls small cell lung cancer (SCLC) neuroendocrine plasticity by binding and destabilizing SOX2 and INSM1 mRNAs, two transcription factors required for SCLC neuroendocrine differentiation. LSD1 binds and represses ZFP36L1; upon LSD1 inhibition, ZFP36L1 expression is restored, blocking the neuroendocrine phenotype and inducing a non-neuroendocrine inflammatory phenotype. ZFP36L1 was identified as required for LSD1 inhibitor sensitivity in a genome-wide CRISPR/Cas9 screen. Genome-wide CRISPR/Cas9 loss-of-function screen, ZFP36L1 forced expression, RNA-IP demonstrating ZFP36L1 binding to SOX2/INSM1 mRNAs, mRNA stability assays, LSD1 ChIP Nature communications High 36008402
1996 The cMG1 gene (later identified as ZFP36L1) is a primary response gene induced 2- to 6-fold by mitogens including EGF, angiotensin II, serum, and insulin in a rat intestinal epithelial cell line. Cyclic AMP-elevating agents blocked EGF-induced cMG1 mRNA increase, and depletion of protein kinase C blocked AII- but not EGF-induced increases, indicating that both PKC-dependent and PKC-independent signaling pathways stimulate ZFP36L1 expression. Northern blot mRNA quantification, PKC depletion, cAMP signaling inhibition, differential mitogen stimulation FEBS letters Low 1628738
1996 Berg36 (ZFP36L1) immediate early gene expression is induced by calcium ionophore in Ramos human B cells, and antisense blockade of Berg36 expression partially inhibited ionophore-induced apoptosis, implicating ZFP36L1 as a requirement for apoptosis induced through calcium signaling in B cells. IL-4 rescue from apoptosis was accompanied by inhibition of Berg36 expression. Antisense oligonucleotide knockdown, apoptosis assays, IL-4 and calcium ionophore treatment of Ramos B cells European journal of immunology Low 8898945
2011 The TIS11 family members (ZFP36, ZFP36L1/BRF-1, ZFP36L2/BRF-2) bind ARE-containing mRNAs and promote their rapid degradation through multiple mechanisms: they recruit deadenylases (CCR4-NOT, PARN), decapping enzymes (DCP1/2), and exonucleases (XRN1, exosome), and their activity is regulated by phosphorylation (MK2, PKB), protein stability (proteasomal degradation), 14-3-3 binding, and subcellular localization. Review synthesizing co-IP, in vitro decay, phosphorylation, and localization studies from multiple labs Wiley interdisciplinary reviews. RNA Medium 21278925
2018 ZFP36L1 and ZFP36L2 act redundantly in myogenesis. Mice with conditional double KO of Zfp36l1 and Zfp36l2 in Pax7-expressing satellite cells had reduced body weight, reduced skeletal muscle mass, fewer satellite cells, and impaired muscle regeneration following cardiotoxin injury. Single KO of either gene alone did not produce the muscle phenotype, demonstrating functional redundancy. Single and double conditional KO mice (Pax7-Cre), immunostaining of muscle sections, cardiotoxin injury regeneration model, satellite cell quantification Skeletal muscle High 30526691

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature 3725 23128233
2011 Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature 2101 21833088
2005 Towards a proteome-scale map of the human protein-protein interaction network. Nature 2090 16189514
2010 Genome-wide meta-analysis increases to 71 the number of confirmed Crohn's disease susceptibility loci. Nature genetics 2036 21102463
2012 Insights into RNA biology from an atlas of mammalian mRNA-binding proteins. Cell 1718 22658674
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2009 Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes. Nature genetics 1382 19430480
2009 A census of human transcription factors: function, expression and evolution. Nature reviews. Genetics 1191 19274049
2010 Multiple common variants for celiac disease influencing immune gene expression. Nature genetics 801 20190752
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
1995 Termination of translation in eukaryotes is governed by two interacting polypeptide chain release factors, eRF1 and eRF3. The EMBO journal 487 7664746
2013 Identification of 23 new prostate cancer susceptibility loci using the iCOGS custom genotyping array. Nature genetics 463 23535732
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2005 Recruitment and activation of mRNA decay enzymes by two ARE-mediated decay activation domains in the proteins TTP and BRF-1. Genes & development 410 15687258
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1995 The products of the SUP45 (eRF1) and SUP35 genes interact to mediate translation termination in Saccharomyces cerevisiae. The EMBO journal 406 7556078
1996 Normalization and subtraction: two approaches to facilitate gene discovery. Genome research 401 8889548
2000 The crystal structure of human eukaryotic release factor eRF1--mechanism of stop codon recognition and peptidyl-tRNA hydrolysis. Cell 372 10676813
1999 Mutations in the highly conserved GGQ motif of class 1 polypeptide release factors abolish ability of human eRF1 to trigger peptidyl-tRNA hydrolysis. RNA (New York, N.Y.) 280 10445876
2004 Transcriptome characterization elucidates signaling networks that control human ES cell growth and differentiation. Nature biotechnology 266 15146197
2014 Efficient multisite unnatural amino acid incorporation in mammalian cells via optimized pyrrolysyl tRNA synthetase/tRNA expression and engineered eRF1. Journal of the American Chemical Society 223 25350841
1996 Eukaryotic polypeptide chain release factor eRF3 is an eRF1- and ribosome-dependent guanosine triphosphatase. RNA (New York, N.Y.) 214 8634914
2013 Salt-responsive ERF1 regulates reactive oxygen species-dependent signaling during the initial response to salt stress in rice. The Plant cell 207 23800963
2007 TTP and BRF proteins nucleate processing body formation to silence mRNAs with AU-rich elements. Genes & development 200 17369404
2015 A deep proteomics perspective on CRM1-mediated nuclear export and nucleocytoplasmic partitioning. eLife 198 26673895
2009 SMG-8 and SMG-9, two novel subunits of the SMG-1 complex, regulate remodeling of the mRNA surveillance complex during nonsense-mediated mRNA decay. Genes & development 198 19417104
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