Affinage

NRIP1

Nuclear receptor-interacting protein 1 · UniProt P48552

Length
1158 aa
Mass
126.9 kDa
Annotated
2026-06-10
100 papers in source corpus 40 papers cited in narrative 40 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NRIP1 (RIP140) is a ligand-dependent transcriptional corepressor that is recruited to the AF-2 domains of nuclear receptors and orchestrates active gene silencing of metabolic and developmental programs (PMID:7641693, PMID:15155905). It binds the ligand-activated estrogen receptor and a broad panel of nuclear receptors (TR, RAR/RXR, PPAR/RXR, GR, SF-1, TR2, AhR) through multiple LXXLL core motifs and an additional C-terminal receptor-interacting motif, and it competes directly with p160/SRC coactivators for the receptor AF-2 surface (PMID:8887632, PMID:9626662, PMID:11078741, PMID:11278635, PMID:12782406). Although named as a corepressor, on the estrogen receptor it co-occupies enhancers genome-wide with ERα, FOXA1, GATA3 and p300/CBP and is required for ERα complex assembly and ERα-driven transcription and proliferation (PMID:25145671, PMID:23404106). Repression is executed by scaffolding chromatin-modifying machinery: RIP140 assembles CtBP, HDAC3, the histone methyltransferase G9a, DNA methyltransferases and the SWI/SNF ATPase Brm onto target promoters, replacing coactivators and converting chromatin from active to repressive marks (PMID:11509661, PMID:11278635, PMID:17972916, PMID:19778926, PMID:24489122, PMID:26921464). Its corepressor potency and nucleocytoplasmic distribution are governed by a layered post-translational code—MAPK/Erk2 phosphorylation triggering p300 acetylation and enhanced HDAC recruitment, PKCε phosphorylation driving 14-3-3 binding, PRMT1 arginine methylation and CRM1-dependent nuclear export, plus SUMOylation, PLP conjugation and signal-induced ubiquitin-dependent degradation (PMID:11509661, PMID:16093479, PMID:17277785, PMID:18628823, PMID:18211901, PMID:18655826, PMID:22388040, PMID:29339732). In the cytoplasm RIP140 acquires distinct functions, binding AS160 to suppress GLUT4 trafficking and adiponectin secretion and binding perilipin to promote lipolysis (PMID:19945409, PMID:21504789, PMID:21872658). Through these activities RIP140 is a master repressor of oxidative and energy-expenditure gene networks: its loss in mice produces a lean, energy-expending phenotype with derepressed UCP1, mitochondrial biogenesis and fatty-acid oxidation genes in adipose, skeletal muscle and heart, while it is also essential for ovulation, restrains intestinal and breast cancer cell proliferation, and tunes macrophage polarization and osteoclast differentiation (PMID:15155905, PMID:11100122, PMID:16374519, PMID:17767910, PMID:36927960, PMID:24667635, PMID:25145671, PMID:28405613).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1995 High

    Established that NRIP1 is a genuine, ligand-regulated interaction partner of the estrogen receptor, defining it as a candidate nuclear receptor cofactor.

    Evidence In vitro binding, co-immunoprecipitation in cells, and reporter assays with the ER AF-2 domain

    PMID:7641693

    Open questions at the time
    • Did not resolve whether NRIP1 activates or represses transcription
    • Binding interface and motifs not yet mapped
  2. 1996 High

    Mapped two independent receptor-binding sites and showed NRIP1 can bridge receptors to transcriptional machinery, beginning to define its cofactor architecture across multiple nuclear receptors.

    Evidence In vitro pulldown domain mapping plus GAL4-fusion reporter assays in yeast and mammalian cells

    PMID:8887632

    Open questions at the time
    • Direction of transcriptional effect on physiological receptors unsettled
    • Identity of recruited machinery unknown
  3. 2000 High

    Defined NRIP1 as a corepressor that competes with SRC-1 coactivators for nuclear receptor AF-2, and that LXXLL core variants tune receptor affinity and selectivity.

    Evidence GST-pulldown, yeast two-hybrid, competitive binding and peptide inhibition assays on PPAR/RXR and steroid/retinoid receptors

    PMID:11078741 PMID:9626662

    Open questions at the time
    • Repressive effector complexes not identified
    • In vivo relevance not established
  4. 2000 High

    Provided the first in vivo demonstration of an essential, non-redundant physiological role, anchoring NRIP1 corepressor function in ovulation.

    Evidence Nrip1 knockout mice with histological ovarian analysis showing oocyte-release failure

    PMID:11100122

    Open questions at the time
    • Molecular targets driving the ovulation defect not defined
    • Which receptor pathway is dysregulated unclear
  5. 2001 High

    Identified the effector complexes through which NRIP1 represses, showing it recruits CtBP and HDAC3 to nuclear receptor target promoters to reduce histone acetylation.

    Evidence In vitro binding, Co-IP, ChIP for histone acetylation, and motif-deletion mutants on RAR/RXR and CtBP-binding sequences

    PMID:11278635 PMID:11509661

    Open questions at the time
    • Full repertoire of recruited chromatin modifiers incomplete
    • Regulation of complex assembly not yet defined
  6. 2003 Medium

    Defined NRIP1 subnuclear targeting and showed repression requires both LXXLL receptor binding and CtBP interaction, integrating localization with corepressor potency.

    Evidence Immunofluorescence, domain-deletion analysis and co-localization with GR/SMRT, plus extension of corepressor activity to SF-1

    PMID:12773562 PMID:12782406

    Open questions at the time
    • Signals controlling focus-to-domain redistribution not fully resolved
    • SF-1 finding limited to reporter systems
  7. 2004 High

    Established NRIP1 as a physiological brake on adipose energy expenditure, linking its corepressor activity to whole-body metabolism.

    Evidence RIP140 knockout mice with metabolic phenotyping showing leanness, obesity resistance and derepressed UCP1

    PMID:15155905

    Open questions at the time
    • Direct target genes and responsible nuclear receptor not yet pinned
    • Tissue autonomy unresolved at this stage
  8. 2007 High

    Defined the gene networks and partner receptors/coactivators through which NRIP1 controls oxidative metabolism, identifying ERRα dependence and direct PGC-1α antagonism.

    Evidence siRNA, microarray, rescue in null MEFs, metabolic assays, fiber-type-specific muscle genetics, and Co-IP/ChIP on CIDEA

    PMID:16374519 PMID:17767910 PMID:18794372

    Open questions at the time
    • Mechanism of coactivator-corepressor switching at single loci not fully resolved
    • Stoichiometry of PGC-1α antagonism unknown
  9. 2007 High

    Showed NRIP1 acts as a scaffold for both DNA and histone methylation machinery, extending its repressive output to heritable epigenetic silencing of metabolic genes.

    Evidence Bisulfite sequencing and ChIP at the Ucp1 enhancer in null vs. wild-type adipocytes; LC-MS/MS mapping of PLP conjugation enhancing HDAC interaction

    PMID:17277785 PMID:17972916

    Open questions at the time
    • Recruitment order of DNMT/HMT complexes not defined
    • Which signals trigger PLP conjugation in vivo unknown
  10. 2008 High

    Defined a multi-layered post-translational code (phosphorylation→acetylation, SUMOylation) that tunes NRIP1 corepressor potency and its nuclear export.

    Evidence MS phosphosite mapping, kinase/acetyltransferase identification (Erk2/p300), PKCε–14-3-3–PRMT1–CRM1 cascade Co-IPs, SUMO mutagenesis and rescue in null adipocytes

    PMID:16093479 PMID:18211901 PMID:18628823 PMID:18655826

    Open questions at the time
    • Quantitative contribution of each modification in vivo unresolved
    • Crosstalk hierarchy among modifications partially defined
  11. 2009 High

    Discovered a distinct cytoplasmic, non-genomic role for NRIP1 in suppressing insulin-stimulated glucose uptake, mechanistically linking nuclear export to metabolic signaling.

    Evidence Co-IP with AS160, subcellular fractionation, GLUT4 trafficking and glucose uptake assays, and diet-induced obesity mouse model

    PMID:19778926 PMID:19945409

    Open questions at the time
    • How cytoplasmic NRIP1 selects AS160 over other substrates unclear
    • Reversibility of cytoplasmic accumulation in vivo not defined
  12. 2011 High

    Broadened cytoplasmic NRIP1 functions to lipid droplet biology and adiponectin secretion, and connected its muscle metabolic action to AMPK-mediated insulin-independent glucose uptake.

    Evidence Co-IP with perilipin, lipolysis assays, adiponectin ELISA, and null/transgenic soleus muscle with AMPK and UCP1 readouts

    PMID:21504789 PMID:21872658 PMID:22389706

    Open questions at the time
    • Adiponectin secretion finding is Medium-confidence and single-lab
    • Switch between lipolytic and anti-lipogenic roles not fully integrated
  13. 2012 High

    Established signal-induced degradation as a mechanism terminating NRIP1 repression, integrating it into inflammatory and immune gene control.

    Evidence Syk phosphorylation, RelA-adaptor Co-IPs, SCF E3 ligase recruitment, and non-degradable mutant macrophages in endotoxin tolerance assays

    PMID:22388040

    Open questions at the time
    • Generality of degradation across tissues not established
    • Which tolerizable gene set is directly bound unclear
  14. 2014 High

    Repositioned NRIP1 in cancer biology, showing it is required for ERα enhancer complex formation in breast cancer yet suppresses Wnt/β-catenin-driven intestinal proliferation.

    Evidence ChIP-seq co-occupancy with ERα/FOXA1/p300, siRNA proliferation assays, and Rip140-null/transgenic mice with APC transcription and xenograft models

    PMID:20410059 PMID:24489122 PMID:24667635 PMID:25145671

    Open questions at the time
    • Context determinants of coactivator vs. corepressor role on ERα unresolved
    • Direct vs. indirect control of APC transcription not fully dissected
  15. 2017 Medium

    Extended the corepressor mechanism to immune and skeletal homeostasis, defining a TR4-based suppressor complex and degradation-controlled macrophage/osteoclast programs.

    Evidence Co-IP with TR4, macrophage-specific knockdown mice, bone histomorphometry, and CaMKII/ubiquitination-driven degradation polarization assays

    PMID:25528964 PMID:26921464 PMID:28405613 PMID:29339732

    Open questions at the time
    • Several findings (DNMT3b, atherosclerosis, M2 polarization) are Medium-confidence single-lab
    • Direct osteoclastogenic target genes incompletely mapped
  16. 2023 High

    Demonstrated that NRIP1 governs a cardiac fuel-metabolism and contractility transcriptional network, with loss conferring protection against heart failure.

    Evidence Striated-muscle- and cardiac-specific Nrip1 knockout mice, pressure-overload+MI heart failure model, RNA-seq/ChIP-seq, and metabolic flux assays implicating ERR and MEF2 enhancers

    PMID:36927960

    Open questions at the time
    • Direct NRIP1-bound cardiac enhancers vs. indirect effects not fully separated
    • Therapeutic window of cardiac NRIP1 inhibition undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved what determines NRIP1's context-dependent switch between corepressor, ERα-complex-assembly cofactor, and cytoplasmic signaling regulator, and how the post-translational code is integrated quantitatively in vivo.
  • No structural model of full-length NRIP1 in receptor/chromatin complexes
  • Cell-type rules dictating activator vs. repressor behavior unknown
  • Human disease genetics not established in this corpus

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0060090 molecular adaptor activity 5 GO:0098772 molecular function regulator activity 4 GO:0042393 histone binding 2
Localization
GO:0005634 nucleus 4 GO:0005654 nucleoplasm 4 GO:0005829 cytosol 3 GO:0005811 lipid droplet 1
Pathway
R-HSA-1430728 Metabolism 5 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-4839726 Chromatin organization 3
Partners
AS160CTBP1ESR1HDAC3PERILIPINPGC-1ΑRELATR4
Complex memberships
ERα enhancer complex (with FOXA1/GATA3/p300/p160)RIP140-CtBP-HDAC3-G9a corepressor complexRIP140-TR4 osteoclast suppressor complex

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 RIP140 (NRIP1) directly interacts in vitro with the ligand-dependent activation domain AF2 of the estrogen receptor; this interaction is increased by estrogen but not by anti-estrogens, and the in vitro binding capacity of mutant receptors correlates with their ability to stimulate transcription. RIP140 also co-immunoprecipitates with ER in intact cells and modulates ER transcriptional activity in the presence of estrogen. In vitro binding assay, co-immunoprecipitation in intact cells, transient transfection reporter assay The EMBO journal High 7641693
1996 RIP140 contains two distinct binding sites (site 1 and site 2) that independently interact with the ligand-binding domain of the estrogen receptor both in solution and when the receptor is bound to DNA; both sites interact with thyroid hormone and retinoic acid receptors, while retinoid X receptor interaction is mediated primarily by site 1. When fused to heterologous DNA-binding domains, RIP140 stimulates transcription in yeast and mammalian cells, suggesting it bridges receptors to the basal transcription machinery. In vitro binding/pulldown mapping, reporter gene assays in yeast and mammalian cells Molecular and cellular biology High 8887632
1998 RIP140 forms ternary complexes with PPAR/RXR heterodimers in the presence of RXR ligands, shows high affinity for the RXR subunit, and generally down-regulates nuclear receptor activity in mammalian cells. In vitro binding of RIP140 and SRC-1 to nuclear receptors is competitive, and RIP140 specifically down-regulates coactivation by SRC-1, suggesting it acts as an indirect inhibitor of AF-2 by competing with coactivators. GST-pulldown, yeast two-hybrid, mammalian cell co-transfection, competitive binding assay Molecular endocrinology High 9626662
1998 RIP140 interacts with the ligand-binding domain of orphan receptor TR2 via LXXLL motifs; the TR2 AF-2 region mediates the interaction. RIP140 functions as a corepressor for TR2 and suppresses RA-receptor-mediated RA induction. Co-immunoprecipitation and GFP nuclear translocation experiments confirmed the RIP140–TR2 interaction in vivo. Yeast two-hybrid, domain mapping, GAL4 reporter, co-immunoprecipitation, GFP nuclear translocation Molecular and cellular biology High 9774688
1999 RIP140 interacts with the aryl hydrocarbon receptor (AhR) but not with ARNT, both in vitro and in cells. The AhR interaction is mediated by its transactivation domain Q-rich subdomain, and the RIP140 interaction domain maps to residues 154–350, distinct from the ER-binding domain. LXXLL motifs are not required for RIP140 binding to AhR. RIP140 enhanced TCDD-mediated dioxin response element-driven reporter gene activity. Co-immunoprecipitation, co-localization assays, domain mapping, reporter gene assay in three cell lines The Journal of biological chemistry High 10428779
1999 RIP140 antagonizes all tested glucocorticoid receptor (GR)-mediated responses, including activation through classical GRE, synergistic effects on AP-1 and Pbx1/HOXB1 elements, gene repression through negative GRE, and NF-κB crosstalk. This requires the GR ligand-binding domain and a GR–RIP140 interaction demonstrated by GST pull-down. Overexpression of coactivator TIF2 partially overcomes RIP140 repression through competition for GR binding. GST pull-down, transient transfection reporter assays, competitive overexpression The Journal of biological chemistry Medium 10364267
2000 LXXLL core motif sequences (8-amino-acid cores) in RIP140 mediate ligand-dependent binding to nuclear receptor ligand-binding domains; variant residues at positions -1 and +2 relative to the first conserved leucine influence affinity and selectivity for steroid and retinoid receptors, as demonstrated by peptide inhibition assays and yeast two-hybrid assays with defined point mutations. Peptide inhibition assay, yeast two-hybrid with mutant LXXLL core motifs The Journal of biological chemistry High 11078741
2001 CtBP interacts with RIP140 in vitro and in vivo through the sequence PIDLSCK in the N-terminal third of RIP140. Acetylation of the lysine residue in this motif by p300/CBP dramatically reduces CtBP binding. Mutation of this lysine to glutamine decreases CtBP binding in vivo and abolishes transcriptional repression, revealing that p300/CBP-mediated acetylation disrupts the RIP140–CtBP complex and derepresses nuclear hormone receptor-regulated genes. In vitro binding, co-immunoprecipitation, acetylation-specific antibody, site-directed mutagenesis, reporter gene assay Molecular and cellular biology High 11509661
2001 RIP140 interacts with retinoic acid receptor/RXR in a ligand-dependent manner through a novel C-terminal motif (LTKTNPILYYMLQK). RA induces co-immunoprecipitation of HDAC3 with RAR/RXR only in the presence of wild-type RIP140 (not C-terminal motif-deleted RIP140), and this is associated with decreased histone acetylation on RA response element-containing promoters. Domain mapping/mutagenesis, co-immunoprecipitation, chromatin immunoprecipitation (histone acetylation) The Journal of biological chemistry High 11278635
2001 14-3-3 proteins interact with the nuclear receptor corepressor RIP140. In transfection assays, 14-3-3 enhances GR transactivation while RIP140 antagonizes this effect. Co-localization studies show that 14-3-3 can export RIP140 out of the nucleus and alter its intranuclear localization, providing a mechanism for enhanced glucocorticoid responsiveness via nuclear depletion of this corepressor. Co-immunoprecipitation, co-localization imaging, transfection reporter assays Molecular endocrinology Medium 11266503
2003 In the absence of ligand-activated GR, RIP140 is localized in small nuclear foci targeted by a 40-amino-acid sequence. The focus-targeting domain overlaps with a CtBP-binding sequence but CtBP interaction is not required for focus localization. Upon GR ligand binding, RIP140 is redistributed to large nuclear domains, requiring RIP140 corepressor-activity regions and the GR DNA-binding domain. Full corepressor activity requires both C-terminal receptor-binding LXXLL motifs and CtBP interaction. Immunofluorescence/subcellular localization, domain-deletion analysis, co-localization with GR and SMRT, mutant functional assays Molecular and cellular biology High 12773562
2004 Mice devoid of RIP140 are lean, resist high-fat diet-induced obesity and hepatic steatosis, and have increased oxygen consumption. RIP140 absence leads to markedly increased UCP1 expression in white adipose tissue and reduced expression of certain lipogenic enzymes, establishing RIP140 as a ligand-dependent transcriptional repressor essential for maintaining energy storage vs. expenditure balance in adipose tissue. RIP140 knockout mouse model, gene expression analysis, metabolic phenotyping PNAS High 15155905
2000 Nrip1 (RIP140) null female mice are infertile due to complete failure of mature follicles to release the oocyte at ovulation, while luteinization proceeds normally. This establishes a specific requirement for the corepressor activity of RIP140 in coordinating ovarian function for oocyte release. Nrip1 knockout mouse model, histological analysis of ovarian phenotype Nature medicine High 11100122
2005 RIP140 depletion by siRNA in 3T3-L1 adipocytes upregulates clusters of genes in glucose uptake, glycolysis, TCA cycle, fatty acid oxidation, mitochondrial biogenesis, and oxidative phosphorylation. Re-expression of RIP140 in RIP140-null MEFs downregulates these same genes. RIP140 mechanistically requires nuclear receptor ERRα to regulate hexose uptake and mitochondrial proteins SDHB and CoxVb. RIP140-null mice show enhanced glucose tolerance and insulin responsiveness. siRNA knockdown, Affymetrix microarray, metabolic assays ([14C]glucose oxidation, mitochondrial O2 consumption), RIP140 re-expression in null MEFs, mouse phenotyping The Journal of clinical investigation High 16374519
2005 MAPK-mediated phosphorylation of RIP140 at Thr202 and Thr207 (in the N-terminal repression domain) enhances its co-repressive activity through increased recruitment of histone deacetylases (HDACs). Phospho-mimetic mutations at these residues convert RIP140 to a more potent repressor resistant to MAPK inhibitor, while dephosphorylation-mimetic mutations impair HDAC recruitment and repressive activity. Mass spectrometry phosphosite identification, site-directed mutagenesis, HDAC co-immunoprecipitation, reporter gene assays, MAPK inhibitor treatment Molecular & cellular proteomics High 16093479
2007 RIP140 is expressed in a fiber type-specific manner in skeletal muscle. Low RIP140 promotes while increased expression suppresses formation of oxidative fibers. Genes involved in fatty-acid oxidation, oxidative phosphorylation, and mitochondrial biogenesis are upregulated in RIP140-null muscle. Changes in gene expression are intrinsic to muscle cells and nuclear receptor-regulated genes are direct targets for repression by RIP140. RIP140 null, heterozygous, and transgenic mouse models, gene expression profiling, cultured myofiber analysis Cell metabolism High 17767910
2007 RIP140 directly interacts with PGC-1α and suppresses its transcriptional activity. Both proteins regulate CIDEA expression via estrogen-related receptor alpha and NRF-1 binding sites on the CIDEA promoter. RIP140 represses while PGC-1α induces CIDEA expression, providing a direct antagonism between corepressor and coactivator via a nuclear receptor-dependent and -independent pathway. Co-immunoprecipitation (RIP140–PGC-1α direct interaction), promoter luciferase assays, chromatin immunoprecipitation, expression analysis in brown adipocytes Molecular and cellular biology High 18794372
2007 RIP140 is essential for both DNA and histone methylation to maintain repression of the Ucp1 gene in white adipocytes. RIP140 promotes assembly of DNA methyltransferases and histone methyltransferases (HMTs) on the Ucp1 enhancer, leading to methylation of specific CpG residues and histones (evidenced by bisulfite genomic sequencing and ChIP), functioning as a scaffold for epigenetic repression machinery. Bisulfite genomic sequencing, chromatin immunoprecipitation, RIP140 null vs. wild-type adipocyte comparison The EMBO journal High 17972916
2007 Pyridoxal 5'-phosphate (PLP, active form of vitamin B6) conjugates RIP140 at Lys613 (mapped by LC-ESI-MS/MS). This modification enhances RIP140 transcriptional corepressive activity and promotes its nuclear retention, attributed to increased interaction of PLP-modified RIP140 with histone deacetylases. LC-ESI-MS/MS modification site mapping, co-immunoprecipitation (HDAC interaction), reporter assays, adipocyte differentiation assay Nature chemical biology High 17277785
2008 PKCε phosphorylates RIP140 at Ser-102 and Ser-1003, which synergistically stimulates 14-3-3 binding; 14-3-3 then recruits protein arginine methyltransferase 1 (PRMT1) to methylate RIP140 arginine residues. Methylated RIP140 preferentially recruits exportin 1 (CRM1) for nuclear export, reducing nuclear gene-repressive activity. Phosphorylation-deficient RIP140 rescues fat accumulation defects in RIP140-null adipocytes more effectively than phospho-mimetic, cytoplasm-localizing RIP140. Site-directed mutagenesis, co-immunoprecipitation (PKCε, 14-3-3, PRMT1, exportin 1), subcellular fractionation, rescue experiments in null adipocytes PloS one High 18628823
2008 SUMOylation of RIP140 at two conserved lysines (Lys756 in RD3 and Lys1154 in RD4) modulates its transcriptional repressor function. SUMO-1 is more efficiently conjugated than SUMO-2/3. Mutation of these SUMOylation sites compromises RIP140 corepressor activity, blunts repression of ERα-dependent transcription, and alters subnuclear distribution of RIP140. In vivo SUMOylation assay, site-directed mutagenesis (Lys756/1154), reporter gene assays, immunofluorescence localization The Journal of biological chemistry High 18211901
2008 p300 is the specific lysine acetyltransferase and Erk2 the specific kinase for RIP140 in adipocytes. Erk2 phosphorylates Thr202/Thr207, which recruits p300 for lysine acetylation of Lys158/Lys287. This phosphorylation→acetylation cascade enhances RIP140 gene-repressive activity. Acetylation-deficient RIP140 fails to rescue fat accumulation defects in RIP140-null cultures whereas phospho-mimetic RIP140 can. In vivo kinase/acetyltransferase identification, site-directed mutagenesis, co-immunoprecipitation, adipocyte rescue experiments Cellular signalling High 18655826
2009 Cytoplasmic RIP140 (exported following PKCε phosphorylation and arginine methylation) interacts with Akt substrate AS160 and impedes Akt-mediated phosphorylation of AS160, thereby reducing GLUT4 trafficking and glucose uptake in adipocytes. This pathway is activated in epididymal adipocytes of diet-induced obese mice where nuclear PKCε is activated and cytoplasmic RIP140 is elevated. Co-immunoprecipitation (RIP140–AS160), subcellular fractionation, GLUT4 trafficking assay, glucose uptake assay, diet-induced obesity mouse model Cell metabolism High 19945409
2009 During T3-mediated repression of Crabp1 gene in differentiating adipocytes, RIP140 is required for the repression. RIP140 replaces coactivators GRIP1 and PCAF on the basal promoter and forms a repressive complex with CtBP1, HDAC3, and histone methyltransferase G9a. This is associated with loss of active chromatin marks (H3-Ac, H3K4-me3) and gain of repressive marks (H3K9-me3, H3K27-me3) and recruitment of HP1α, HP1γ, and H1 to the promoter. Chromatin immunoprecipitation, bisulfite sequencing, co-immunoprecipitation, gene expression analysis in differentiating 3T3-L1 cells Nucleic acids research High 19778926
2011 Cytoplasmic RIP140 directly interacts with perilipin on lipid droplets in adipocytes (triggered by elevated diacylglycerol). This interaction facilitates perilipin's recruitment of hormone-sensitive lipase (HSL) to lipid droplets and promotes ATGL/CGI-58 complex formation, ultimately enhancing lipolysis. Blocking cytoplasmic RIP140 accumulation reduces basal and isoproterenol-stimulated lipolysis. Co-immunoprecipitation (RIP140–perilipin, perilipin–HSL, ATGL–CGI-58), lipid droplet fractionation, lipolysis assay, siRNA knockdown Cellular signalling High 21504789
2011 Cytoplasmic RIP140 regulates adiponectin secretion via interaction with AS160 without affecting adiponectin production or oligomerization. Knockdown of RIP140 or its nuclear export trigger PKCε promotes adiponectin secretion and consequently enhances glucose uptake in C2C12 cells and reduces gluconeogenesis in HepG2 cells. Co-immunoprecipitation (RIP140–AS160), ELISA (adiponectin secretion), siRNA knockdown, conditioned media experiments, neutralizing antibody Cellular signalling Medium 21872658
2012 LPS stimulates Syk kinase-mediated tyrosine phosphorylation of RIP140, which promotes interaction of NF-κB subunit RelA with RIP140, leading to recruitment of E3 ligase SCF complex that degrades RIP140 to inactivate proinflammatory cytokine genes. Macrophages expressing non-degradable RIP140 resist establishment of endotoxin tolerance for specific tolerizable genes, identifying RelA as an adaptor for SCF-mediated RIP140 degradation. Co-immunoprecipitation (RIP140–RelA, RIP140–SCF), phospho-tyrosine detection, non-degradable RIP140 mutant macrophages, LPS tolerance assays Nature immunology High 22388040
2010 RIP140 represses E2F1 transactivation on various E2F target promoters and inhibits expression of E2F1 target genes (e.g., CCNE1, CCNB2). Physical interaction between RIP140 and E2F1 was demonstrated by GST pull-down and co-immunoprecipitation. Increasing RIP140 levels reduces the proportion of cells in S phase in human cell lines. GST pull-down, co-immunoprecipitation, ChIP, transfection reporter assays, FACS cell cycle analysis Clinical cancer research High 20410059
2014 RIP140 ChIP-seq reveals that it shares >80% of binding sites with ERα, co-localizing with FOXA1, GATA3, p300, CBP, and p160 family members at H3K4me1-demarcated enhancer regions. RIP140 is required for ERα complex formation and ERα-mediated gene expression and ERα-dependent breast cancer cell proliferation. ChIP-seq (RIP140, ERα), siRNA knockdown, gene expression analysis, cell proliferation assay Cancer research High 25145671
2014 RIP140 inhibits intestinal epithelial cell proliferation and promotes APC transcription, inhibiting β-catenin activation and target gene expression. RIP140 overexpression strongly represses colon cancer cell proliferation in vitro and in vivo. In murine tissues and human cancer cells, RIP140 stimulates APC transcription. Rip140-null mice, RIP140 overexpressing transgenic mice, xenograft tumor model, gene expression analysis, reporter assays The Journal of clinical investigation High 24667635
2014 RIP140 in adipocyte chromatin remodeling requires its lysine acetylation for recruiting Brm (SWI/SNF ATPase subunit). RA-induced coordinated repressive chromatin-remodeling of Nanog and Oct4 gene loci in embryonic stem cells requires RAR-α, RIP140, and Brm. Chromatin immunoprecipitation, nucleosome positioning assay, RIP140 acetylation mutant, co-immunoprecipitation with Brm Nucleic acids research Medium 24489122
2014 RIP140 reduces expression of reverse cholesterol transport genes ABCA1 and ABCG1 in macrophages, enhancing foam cell formation. In macrophage-specific RIP140 knockdown crossed with ApoE null mice, high-cholesterol diet-induced atherosclerosis is significantly ameliorated. Gene expression analysis, macrophage-specific RIP140 knockdown transgenic mouse, ApoE null atherosclerosis model, lipid accumulation assay Journal of molecular and cellular cardiology Medium 25528964
2017 RIP140 in osteoclast precursors inhibits osteoclast differentiation by forming a transcription-suppressor complex with testicular receptor 4 (TR4) to repress osteoclastogenic genes. Syk-stimulated RIP140 protein degradation terminates this suppressive activity. Monocyte/macrophage-specific RIP140 knockdown results in increased bone resorption and reduced bone formation. Co-immunoprecipitation (RIP140–TR4), macrophage-specific RIP140 KD mice, bone histomorphometry, Syk-mediated degradation assay, osteoclast differentiation assay JCI insight High 28405613
2018 Glyburide stimulates Ca2+/calmodulin-dependent protein kinase II (CaMKII) activation, which triggers specific ubiquitination of RIP140, leading to its degradation. This RIP140 degradation enhances M2 macrophage polarization and anti-inflammatory response. CaMKII activation assay, ubiquitination assay, RIP140 degradation measurement, macrophage polarization assay, wound healing model Scientific reports Medium 29339732
2023 RIP140 (encoded by Nrip1) suppresses a transcriptional regulatory network controlling cardiac fuel metabolism and contractile function. Striated muscle-specific RIP140 deficiency increases expression of genes involved in mitochondrial energy metabolism and contractile function. Cardiac-specific RIP140 deficiency protects against heart failure from pressure overload combined with myocardial infarction. Genomic enhancers activated by RIP140 deficiency are enriched for ERR and MEF2 binding motifs. Loss of RIP140 in heart augments triacylglyceride turnover and fatty acid utilization. Striated muscle-specific and cardiac-specific Nrip1 knockout mice, pressure overload + MI heart failure model, RNA-seq, ChIP-seq, metabolic flux assays The Journal of clinical investigation High 36927960
2011 RIP140 null soleus muscle shows increased GLUT4 trafficking and glucose uptake with no change in Akt activity, but with increased AMPK phosphorylation/activity and elevated UCP1 expression and mitochondrial uncoupling, revealing a pathway controlling insulin-independent glucose uptake through UCP1-mediated AMPK activation. RIP140 transgenic soleus shows reduced AMPK phosphorylation/activity. RIP140 null and transgenic mouse models, GLUT4 trafficking assay, glucose uptake assay, AMPK phosphorylation measurement, UCP1 expression, mitochondrial uncoupling assay PloS one High 22389706
2016 RIP140 interacts with DNMT3b in macrophages (shown by co-immunoprecipitation). LPS stimulation increases PPARγ promoter methylation and inhibits its transcriptional activity; RIP140 knockdown reduces DNMT3b-mediated PPARγ promoter methylation and restores PPARγ activity. Co-immunoprecipitation (RIP140–DNMT3b), bisulfite pyrosequencing, PPARγ promoter methylation and activity assays, siRNA knockdown in RAW264.7 cells Pulmonary pharmacology & therapeutics Medium 26921464
2022 RIP140 reduces transcription of the glucose transporter GLUT3 gene by inhibiting the transcriptional activity of HIF-2α in cooperation with p53, thereby suppressing glycolysis-dependent breast cancer cell proliferation. Cell proliferation assays, metabolic assays, reporter gene assays, siRNA knockdown, RIP140 overexpression, co-immunoprecipitation/interaction with HIF-2α and p53 Cellular and molecular life sciences Medium 35501580
2003 RIP140 interacts with steroidogenic factor 1 (SF-1) through its AF-2 domain; the C-terminal region of RIP140 containing 4 LXXLL motifs shows the strongest interaction. RIP140 acts as a potent corepressor of SF-1-dependent transcription from the CYP17 CRS2 element and counteracts SRC/p160 coactivators. The inhibitory effect is partially reversed by trichostatin A, indicating HDAC involvement. GST pull-down, domain mapping, reporter gene assays in multiple cell types, trichostatin A treatment Molecular and cellular endocrinology Medium 12782406
2013 RIP140 is required in both mammary epithelial and stromal compartments for ductal elongation during puberty and acts as a co-regulator with ERα to directly regulate expression of amphiregulin (Areg), the progesterone receptor (Pgr), and Stat5a, based on genome-wide ERα ChIP-seq and selective ChIP verification of RIP140 co-occupancy. RIP140-null and transgenic mouse models, tissue recombination experiments, ChIP-seq (ERα), ChIP (RIP140 co-occupancy), gene expression analysis Development High 23404106

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 Nuclear factor RIP140 modulates transcriptional activation by the estrogen receptor. The EMBO journal 664 7641693
2004 Nuclear receptor corepressor RIP140 regulates fat accumulation. Proceedings of the National Academy of Sciences of the United States of America 312 15155905
2008 Chloroplastic protein NRIP1 mediates innate immune receptor recognition of a viral effector. Cell 289 18267075
2005 Suppression of oxidative metabolism and mitochondrial biogenesis by the transcriptional corepressor RIP140 in mouse adipocytes. The Journal of clinical investigation 191 16374519
1998 A regulatory role for RIP140 in nuclear receptor activation. Molecular endocrinology (Baltimore, Md.) 190 9626662
2007 The transcriptional corepressor RIP140 regulates oxidative metabolism in skeletal muscle. Cell metabolism 164 17767910
2000 The nuclear receptor co-repressor nrip1 (RIP140) is essential for female fertility. Nature medicine 153 11100122
2008 A functional interaction between RIP140 and PGC-1alpha regulates the expression of the lipid droplet protein CIDEA. Molecular and cellular biology 136 18794372
2000 Core LXXLL motif sequences in CREB-binding protein, SRC1, and RIP140 define affinity and selectivity for steroid and retinoid receptors. The Journal of biological chemistry 136 11078741
2001 Acetylation of nuclear hormone receptor-interacting protein RIP140 regulates binding of the transcriptional corepressor CtBP. Molecular and cellular biology 126 11509661
1999 Differential recruitment of coactivator RIP140 by Ah and estrogen receptors. Absence of a role for LXXLL motifs. The Journal of biological chemistry 121 10428779
1996 RIP-140 interacts with multiple nuclear receptors by means of two distinct sites. Molecular and cellular biology 117 8887632
1998 Cloning and characterization of mouse RIP140, a corepressor for nuclear orphan receptor TR2. Molecular and cellular biology 113 9774688
2015 miR-30 promotes thermogenesis and the development of beige fat by targeting RIP140. Diabetes 112 25576051
2006 Metabolic regulation by the nuclear receptor corepressor RIP140. Trends in endocrinology and metabolism: TEM 91 16815031
2012 NF-κB-mediated degradation of the coactivator RIP140 regulates inflammatory responses and contributes to endotoxin tolerance. Nature immunology 89 22388040
2007 RIP140 directs histone and DNA methylation to silence Ucp1 expression in white adipocytes. The EMBO journal 89 17972916
1999 Receptor interacting protein RIP140 inhibits both positive and negative gene regulation by glucocorticoids. The Journal of biological chemistry 87 10364267
2013 Distinct functions for RIP140 in development, inflammation, and metabolism. Trends in endocrinology and metabolism: TEM 66 23742741
2007 Vitamin B6 conjugation to nuclear corepressor RIP140 and its role in gene regulation. Nature chemical biology 63 17277785
2001 Regulation of glucocorticoid receptor activity by 14--3-3-dependent intracellular relocalization of the corepressor RIP140. Molecular endocrinology (Baltimore, Md.) 62 11266503
2007 Role of RIP140 in metabolic tissues: connections to disease. FEBS letters 54 18023280
1999 Estrogen receptor domains E and F: role in dimerization and interaction with coactivator RIP-140. Molecular endocrinology (Baltimore, Md.) 54 9973258
2020 Circular RNA circNTRK2 facilitates the progression of esophageal squamous cell carcinoma through up-regulating NRIP1 expression via miR-140-3p. Journal of experimental & clinical cancer research : CR 53 32653032
2006 RIP140 expression is stimulated by estrogen-related receptor alpha during adipogenesis. The Journal of biological chemistry 52 16923809
2001 Transcriptional activation of the nuclear receptor corepressor RIP140 by retinoic acid: a potential negative-feedback regulatory mechanism. Biochemical and biophysical research communications 51 11467847
2008 RNAi screens reveal novel metabolic regulators: RIP140, MAP4k4 and the lipid droplet associated fat specific protein (FSP) 27. Acta physiologica (Oxford, England) 50 18171433
2014 NRIP1/RIP140 siRNA-mediated attenuation counteracts mitochondrial dysfunction in Down syndrome. Human molecular genetics 48 24698981
2009 A negative regulatory pathway of GLUT4 trafficking in adipocyte: new function of RIP140 in the cytoplasm via AS160. Cell metabolism 48 19945409
2000 Environmental estrogens induce transcriptionally active estrogen receptor dimers in yeast: activity potentiated by the coactivator RIP140. Environmental health perspectives 48 10656848
2010 The transcriptional coregulator RIP140 represses E2F1 activity and discriminates breast cancer subtypes. Clinical cancer research : an official journal of the American Association for Cancer Research 46 20410059
2006 Transcriptional regulation of the human NRIP1/RIP140 gene by estrogen is modulated by dioxin signalling. Molecular pharmacology 46 16391242
2003 Regulation of subnuclear localization is associated with a mechanism for nuclear receptor corepression by RIP140. Molecular and cellular biology 46 12773562
2018 CRISPR-delivery particles targeting nuclear receptor-interacting protein 1 (Nrip1) in adipose cells to enhance energy expenditure. The Journal of biological chemistry 44 30190322
2014 Reducing RIP140 expression in macrophage alters ATM infiltration, facilitates white adipose tissue browning, and prevents high-fat diet-induced insulin resistance. Diabetes 44 24969109
2013 The transcriptional co-factor RIP140 regulates mammary gland development by promoting the generation of key mitogenic signals. Development (Cambridge, England) 44 23404106
2010 Role of nuclear receptor corepressor RIP140 in metabolic syndrome. Biochimica et biophysica acta 44 21193034
2006 The nuclear receptor transcriptional coregulator RIP140. Nuclear receptor signaling 44 17088940
2006 Negative regulation of hormone signaling by RIP140. The Journal of steroid biochemistry and molecular biology 43 17056252
2014 RIP140 increases APC expression and controls intestinal homeostasis and tumorigenesis. The Journal of clinical investigation 42 24667635
2001 Ligand-dependent formation of retinoid receptors, receptor-interacting protein 140 (RIP140), and histone deacetylase complex is mediated by a novel receptor-interacting motif of RIP140. The Journal of biological chemistry 42 11278635
2008 SUMOylation modulates the transcription repressor function of RIP140. The Journal of biological chemistry 40 18211901
2012 Roles of transcriptional corepressor RIP140 and coactivator PGC-1α in energy state of chronically infarcted rat hearts and mitochondrial function of cardiomyocytes. Molecular and cellular endocrinology 39 22503866
2005 Role of the RIP140 corepressor in ovulation and adipose biology. The Journal of endocrinology 39 15817822
2005 Regulation of co-repressive activity of and HDAC recruitment to RIP140 by site-specific phosphorylation. Molecular & cellular proteomics : MCP 39 16093479
2021 CircRNA NRIP1 promotes papillary thyroid carcinoma progression by sponging mir-195-5p and modulating the P38 MAPK and JAK/STAT pathways. Diagnostic pathology 37 34689819
2014 RIP140 represses the "brown-in-white" adipocyte program including a futile cycle of triacylglycerol breakdown and synthesis. Molecular endocrinology (Baltimore, Md.) 37 24479876
2020 circ-NRIP1 Promotes Glycolysis and Tumor Progression by Regulating miR-186-5p/MYH9 Axis in Gastric Cancer. Cancer management and research 36 32765095
2022 Fusion gene detection by RNA-sequencing complements diagnostics of acute myeloid leukemia and identifies recurring NRIP1-MIR99AHG rearrangements. Haematologica 35 34134471
2008 Post-translational modifications of nuclear co-repressor RIP140: a therapeutic target for metabolic diseases. Current medicinal chemistry 35 18288993
2023 ALKBH5-induced circular RNA NRIP1 promotes glycolysis in thyroid cancer cells by targeting PKM2. Cancer science 34 36851875
2008 Modulation of lysine acetylation-stimulated repressive activity by Erk2-mediated phosphorylation of RIP140 in adipocyte differentiation. Cellular signalling 34 18655826
2015 Suppressing NRIP1 inhibits growth of breast cancer cells in vitro and in vivo. Oncotarget 33 26492163
2013 Negative regulation of estrogen signaling by ERβ and RIP140 in ovarian cancer cells. Molecular endocrinology (Baltimore, Md.) 33 23885094
2011 Aryl hydrocarbon receptor modulation of estrogen receptor α-mediated gene regulation by a multimeric chromatin complex involving the two receptors and the coregulator RIP140. Toxicological sciences : an official journal of the Society of Toxicology 33 22071320
2009 Four and a half LIM domains 1 (FHL1) and receptor interacting protein of 140kDa (RIP140) interact and cooperate in estrogen signaling. The international journal of biochemistry & cell biology 33 19401155
2011 Clenbuterol, a β2-adrenergic agonist, reciprocally alters PGC-1 alpha and RIP140 and reduces fatty acid and pyruvate oxidation in rat skeletal muscle. American journal of physiology. Regulatory, integrative and comparative physiology 32 22071161
2008 PKCepsilon stimulated arginine methylation of RIP140 for its nuclear-cytoplasmic export in adipocyte differentiation. PloS one 31 18628823
2006 Multilocus analysis of estrogen-related genes in Spanish postmenopausal women suggests an interactive role of ESR1, ESR2 and NRIP1 genes in the pathogenesis of osteoporosis. Bone 31 16530497
2003 Negative feedback at the level of nuclear receptor coregulation. Self-limitation of retinoid signaling by RIP140. The Journal of biological chemistry 31 14506269
2018 MicroRNA-548-3p and MicroRNA-576-5p enhance the migration and invasion of esophageal squamous cell carcinoma cells via NRIP1 down-regulation. Neoplasma 30 29940757
2005 Multiple signaling defects in the absence of RIP140 impair both cumulus expansion and follicle rupture. Endocrinology 30 15919748
2021 circ_NRIP1 is oncogenic in malignant development of esophageal squamous cell carcinoma (ESCC) via miR-595/SEMA4D axis and PI3K/AKT pathway. Cancer cell international 29 33957921
2012 Absence of RIP140 reveals a pathway regulating glut4-dependent glucose uptake in oxidative skeletal muscle through UCP1-mediated activation of AMPK. PloS one 29 22389706
2011 Cytoplasmic receptor-interacting protein 140 (RIP140) interacts with perilipin to regulate lipolysis. Cellular signalling 28 21504789
2015 NOP14 suppresses breast cancer progression by inhibiting NRIP1/Wnt/β-catenin pathway. Oncotarget 27 26213846
2000 The impact of differential binding of wild-type RARalpha, PML-, PLZF- and NPM-RARalpha fusion proteins towards transcriptional co-activator, RIP-140, on retinoic acid responses in acute promyelocytic leukemia. Leukemia 27 10637480
2014 Complex formation and function of estrogen receptor α in transcription requires RIP140. Cancer research 26 25145671
2007 Selective repression of retinoic acid target genes by RIP140 during induced tumor cell differentiation of pluripotent human embryonal carcinoma cells. Molecular cancer 26 17880687
2002 Embryo transfer experiments and ovarian transplantation identify the ovary as the only site in which nuclear receptor interacting protein 1/RIP140 action is crucial for female fertility. Endocrinology 26 11796527
2009 RIP140 in thyroid hormone-repression and chromatin remodeling of Crabp1 gene during adipocyte differentiation. Nucleic acids research 25 19778926
2007 Orphan nuclear receptor TR2, a mediator of preadipocyte proliferation, is differentially regulated by RA through exchange of coactivator PCAF with corepressor RIP140 on a platform molecule GRIP1. Nucleic acids research 25 17389641
2005 Limiting effects of RIP140 in estrogen signaling: potential mediation of anti-estrogenic effects of retinoic acid. The Journal of biological chemistry 25 15632153
2018 Glyburide and retinoic acid synergize to promote wound healing by anti-inflammation and RIP140 degradation. Scientific reports 22 29339732
2017 Transcriptional coregulator RIP140: an essential regulator of physiology. Journal of molecular endocrinology 22 28073818
2015 Expression and role of RIP140/NRIP1 in chronic lymphocytic leukemia. Journal of hematology & oncology 22 25879677
2015 The emerging role of the transcriptional coregulator RIP140 in solid tumors. Biochimica et biophysica acta 22 26116758
2014 RIP140 contributes to foam cell formation and atherosclerosis by regulating cholesterol homeostasis in macrophages. Journal of molecular and cellular cardiology 22 25528964
2012 The RIP140 gene is a transcriptional target of E2F1. PloS one 22 22629304
2016 Overexpression and potential roles of NRIP1 in psoriasis. Oncotarget 21 27708240
2004 Retinoids and receptor interacting protein 140 (RIP140) in gene regulation. Current medicinal chemistry 21 15180561
2003 Effects of retinoid ligands on RIP140: molecular interaction with retinoid receptors and biological activity. Biochemistry 21 12549917
2021 Hyperoside Protects HK-2 Cells Against High Glucose-Induced Apoptosis and Inflammation via the miR-499a-5p/NRIP1 Pathway. Pathology oncology research : POR 20 34257594
2006 The nuclear receptor co-repressor RIP140 controls the expression of metabolic gene networks. Biochemical Society transactions 20 17073760
2023 RIP140 deficiency enhances cardiac fuel metabolism and protects mice from heart failure. The Journal of clinical investigation 19 36927960
2019 The circular RNA-NRIP1 plays oncogenic roles by targeting microRNA-505 in the renal carcinoma cell lines. Journal of cellular biochemistry 19 31692056
2014 Coordinated repressive chromatin-remodeling of Oct4 and Nanog genes in RA-induced differentiation of embryonic stem cells involves RIP140. Nucleic acids research 19 24489122
2014 The p65 subunit of NF-κB involves in RIP140-mediated inflammatory and metabolic dysregulation in cardiomyocytes. Archives of biochemistry and biophysics 19 24823858
2011 Negative regulation of adiponectin secretion by receptor interacting protein 140 (RIP140). Cellular signalling 19 21872658
2004 Molecular interaction of retinoic acid receptors with coregulators PCAF and RIP140. Molecular and cellular endocrinology 19 15489004
2022 RIP140 inhibits glycolysis-dependent proliferation of breast cancer cells by regulating GLUT3 expression through transcriptional crosstalk between hypoxia induced factor and p53. Cellular and molecular life sciences : CMLS 18 35501580
2017 RIP140 in monocytes/macrophages regulates osteoclast differentiation and bone homeostasis. JCI insight 18 28405613
2015 M1-M2 balancing act in white adipose tissue browning - a new role for RIP140. Adipocyte 18 26167418
2011 Reductions in RIP140 are not required for exercise- and AICAR-mediated increases in skeletal muscle mitochondrial content. Journal of applied physiology (Bethesda, Md. : 1985) 18 21700896
2003 Characterization of receptor-interacting protein RIP140 in the regulation of SF-1 responsive target genes. Molecular and cellular endocrinology 18 12782406
2018 Deletion of Nrip1 Extends Female Mice Longevity, Increases Autophagy, and Delays Cell Senescence. The journals of gerontology. Series A, Biological sciences and medical sciences 17 29346516
2016 RIP140 down-regulation alleviates acute lung injury via the inhibition of LPS-induced PPARγ promoter methylation. Pulmonary pharmacology & therapeutics 17 26921464
2014 Downregulation of RIP140 in hepatocellular carcinoma promoted the growth and migration of the cancer cells. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 17 25391428
2017 Overexpression of RIP140 suppresses the malignant potential of hepatocellular carcinoma by inhibiting NF‑κB‑mediated alternative polarization of macrophages. Oncology reports 16 28393222
2017 Transcriptional co-regulator RIP140: An important mediator of the inflammatory response and its associated diseases (Review). Molecular medicine reports 15 28586037

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