| 1997 |
N-CoR forms a complex with mSin3 and histone deacetylase mRPD3 (HDAC1), and this complex is required for both nuclear receptor-mediated and Mad-dependent transcriptional repression. The ligand-induced switch from repressor to activator function involves exchange of HDAC-containing complexes for histone acetyltransferase-containing complexes. |
Biochemical co-purification, co-immunoprecipitation, functional repression assays |
Nature |
High |
9139820 9139821
|
| 1997 |
N-CoR interacts with mSin3A/B scaffold proteins and histone deacetylase HD1, providing a molecular basis for Mxi1/Sin3-induced transcriptional repression and tumour suppression in the context of Myc family regulation. |
Co-immunoprecipitation, functional transcriptional repression assays |
Nature |
High |
9139821
|
| 1996 |
N-CoR/RIP13 contains two distinct receptor interaction domains (ID-I and ID-II), each capable of independently binding thyroid hormone receptor (TR) or retinoic acid receptor (RAR); interaction with retinoid X receptor also occurs but is weaker. |
Yeast two-hybrid, mammalian two-hybrid, in vitro direct binding assays |
Molecular endocrinology |
Medium |
8961273
|
| 1998 |
ETO, the fusion partner in t(8;21) acute myeloid leukemia, binds N-CoR through two zinc finger motifs at its C-terminus; N-CoR forms a complex with mSin3A/B and HDAC1, and ETO exploits this complex to repress transcription, providing a mechanism for AML1/ETO-mediated inhibition of AML1 target genes. |
Yeast two-hybrid, co-immunoprecipitation, transcriptional repression assays, deletion mutagenesis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
9724795 9819404
|
| 1998 |
N-CoR and SMRT corepressor complexes are regulated by diverse signal transduction pathways; decreased N-CoR levels correlate with acquisition of tamoxifen resistance, and N-CoR/SMRT complexes act as rate-limiting components in tamoxifen-dependent antagonism of estrogen receptor. |
Transfection assays, co-immunoprecipitation, mouse model of tamoxifen resistance |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
9501191
|
| 1998 |
The BCL-6 POZ domain interacts with N-CoR and SMRT corepressors; this interaction is necessary and sufficient for transcriptional repression by BCL-6; BCL-6 and N-CoR co-localize to punctate nuclear regions; POZ domains from other proteins (PLZF, ZID, GAGA) also interact with N-CoR. |
Yeast two-hybrid, mammalian two-hybrid, co-immunoprecipitation, indirect immunofluorescence co-localization, deletion and point mutagenesis |
Oncogene |
High |
9824158
|
| 1998 |
DAX-1 recruits N-CoR to steroidogenic factor 1 (SF-1), functioning as an adaptor molecule that extends corepressor action to DNA-bound nuclear receptors; naturally occurring AHC mutations of DAX-1 permit SF-1-DAX-1 interaction but markedly diminish N-CoR recruitment. |
Co-immunoprecipitation, mammalian two-hybrid, transcriptional repression assays, analysis of disease mutants |
Molecular and cellular biology |
Medium |
9566914
|
| 1998 |
N-CoR and its splice variants directly interact with basal transcription factors TFIIB, TAFII32, and TAFII70 in vitro and in vivo; N-CoR expression abolishes the functional TFIIB-TAFII32 interaction critical for transcription initiation, suggesting N-CoR locks the basal machinery into a non-functional conformation. |
GST pull-down, co-immunoprecipitation, yeast two-hybrid, transcription functional assays |
Nucleic acids research |
Medium |
9611234
|
| 1998 |
SAP30, a component of the mSin3 complex, binds N-CoR and is required for N-CoR-mediated repression by antagonist-bound estrogen receptor and homeodomain protein Rpx, and for N-CoR suppression of Pit-1 transactivation, but is not required for N-CoR-mediated repression by unliganded RAR or TR — indicating SAP30 is involved in a specific subset of N-CoR complexes. |
Co-immunoprecipitation, transcriptional repression assays with SAP30 mutants |
Molecular cell |
Medium |
9702189
|
| 2000 |
N-CoR exists in two distinct multiprotein complexes (N-CoR-1 and N-CoR-2): N-CoR-1 contains HDAC3, SWI/SNF-related proteins (BRG1, BAF170, BAF155, BAF47/INI1), and corepressor KAP-1; N-CoR-2 contains HDAC1 and HDAC2 and Sin3A complex subunits. KAP-1 and N-CoR co-localize throughout the nucleus. |
Immunoaffinity chromatography, mass spectrometry, Western blotting, indirect immunofluorescence |
The Journal of biological chemistry |
Medium |
11013263
|
| 2000 |
N-CoR contains three receptor interaction domains (IDs), each with a conserved I/LXXII hydrophobic core motif that is required for binding to unliganded TR; the third ID (ID3) may be the most important for TR binding. Substitution of ID isoleucines with leucines does not allow binding to liganded TR, indicating the binding preference for unliganded TR is not determined solely by the identity of conserved hydrophobic residues. |
In vitro binding assays, yeast two-hybrid, mammalian two-hybrid, site-directed mutagenesis |
Molecular endocrinology |
Medium |
11117528
|
| 2000 |
Both SMRT and N-CoR exist in large (~1.5–2 MDa) complexes in HeLa nuclear extracts containing HDAC3 and TBL1 (a WD-40 repeat protein); these complexes bind unliganded thyroid hormone receptors in vitro; injection of antibodies against HDAC3 or SMRT/N-CoR into Xenopus oocytes partially relieves repression by unliganded TR/RXR. |
Conventional and immunoaffinity chromatography, Western blotting, in vitro binding, Xenopus oocyte antibody injection |
The EMBO journal |
High |
10944117
|
| 2001 |
The SMRT and N-CoR corepressors activate HDAC3 through a deacetylase activating domain (DAD) containing one of their SANT motifs; recombinant HDAC3 alone is inactive, but reconstitution with the DAD of either SMRT or N-CoR is necessary and sufficient to activate HDAC3 enzymatic activity; mutations in the DAD that abolish HDAC3 interaction also eliminate HDAC activity reconstitution and the major repression function. |
In vitro reconstitution with purified components, site-directed mutagenesis, HDAC enzymatic assays |
Molecular and cellular biology |
High |
11509652
|
| 2002 |
Class II HDACs (e.g., HDAC4) interact with HDAC3 via N-CoR/SMRT; class II HDACs are enzymatically inactive within the SMRT/N-CoR-HDAC3 complex and do not contribute to its deacetylase activity; class II HDACs regulate transcription by bridging the enzymatically active SMRT/N-CoR-HDAC3 complex to select transcription factors independently of intrinsic HDAC activity. |
In vitro reconstitution, co-immunoprecipitation, HDAC enzymatic assays, suppression of HDAC4-SMRT/N-CoR interaction |
Molecular cell |
High |
11804585
|
| 2002 |
GPS2 is an integral subunit of the N-CoR-HDAC3 complex; GPS2 and TBL1 interact cooperatively with repression domain 1 of N-CoR to form a heterotrimeric structure indirectly linked to HDAC3 via an extended N-CoR SANT domain that activates latent HDAC3 activity; the N-CoR-HDAC3 complex inhibits JNK activation through the associated GPS2 subunit. |
Mass spectrometry, co-immunoprecipitation, structural domain mapping, JNK activation assays |
Molecular cell |
High |
11931768
|
| 2002 |
N-CoR is required for neural stem cell self-renewal; FGF2-treated embryonic cortical progenitors from N-CoR knockout mice display impaired self-renewal and spontaneous differentiation into astroglia-like cells. CNTF-induced astroglia differentiation involves PI3K/Akt1-dependent phosphorylation of N-CoR, causing its redistribution from nucleus to cytoplasm; recruitment of protein phosphatase-1 to a specific binding site on N-CoR exerts a reciprocal effect on N-CoR localization. |
Genetic knockout mouse, live cell fractionation, kinase inhibitor experiments, immunofluorescence localization |
Nature |
High |
12410313
|
| 2002 |
Prohibitin recruits N-CoR and HDAC activity to repress E2F-mediated transcription; prohibitin-mediated repression requires histone deacetylase activity and N-CoR, and correlates with histone deacetylation on promoters. |
Co-immunoprecipitation, transcriptional repression assays, HDAC inhibitor treatment |
Oncogene |
Medium |
12466959
|
| 2002 |
p65-NFκB enhances Notch-mediated activation of the Hes1 promoter by triggering cytoplasmic translocation of the transcriptional corepressor N-CoR, thereby abrogating N-CoR-mediated repression; this mechanism also operates on other promoters repressed by N-CoR containing SRE and AP-1 sites. |
Subcellular fractionation, immunofluorescence, transcriptional reporter assays |
Journal of cell science |
Medium |
11884528
|
| 2003 |
The purified human N-CoR complex contains 10–12 associated proteins; TBL1/TBLR1 associates with N-CoR through two independent interactions (N-terminal region with RD1, C-terminal WD-40 repeats with RD4); TBL1/TBLR1 bind histones H2B and H4 in vitro; siRNA knockdown shows HDAC3 is essential and TBL1/TBLR1 are functionally redundant but essential for repression by unliganded TR. |
Immunoaffinity purification, mass spectrometry, in vitro histone binding, siRNA knockdown, transcriptional repression assays |
The EMBO journal |
High |
12628926
|
| 2003 |
Kaiso, a methyl-CpG-binding BTB/POZ protein, is a component of the human N-CoR complex; the Kaiso/N-CoR complex binds specific CpG-rich sequences in a methylation-dependent manner in vitro; Kaiso targets the N-CoR complex to the MTA2 gene promoter in a methylation-dependent manner in vivo, requiring both Kaiso function and a functional N-CoR deacetylase complex, which mediates histone hypoacetylation and H3K9 methylation. |
Co-immunoprecipitation, in vitro DNA binding with methylated substrates, ChIP, siRNA knockdown |
Molecular cell |
High |
14527417
|
| 2003 |
Endogenous N-CoR, TBL1, and HDAC3 (but not HDAC1, -2, or -4) are recruited to a stably integrated reporter gene repressed by unliganded TR and by orphan receptor RevErb; repression is associated with local histone deacetylation reversed by thyroid hormone. siRNA knockdown of N-CoR markedly reduces TR repression whereas SMRT knockdown has little effect; HDAC3 knockdown markedly reduces repression by both TR and RevErb. |
Chromatin immunoprecipitation (ChIP), siRNA knockdown, transcriptional reporter assays |
Molecular and cellular biology |
High |
12861000
|
| 2003 |
JMJD2A directly interacts with the N-terminal region of N-CoR through a specific NID (N-CoR interaction domain) both in vitro and in vivo; JMJD2A is not a core subunit of the stable N-CoR complex and is not required for TR-mediated repression; JMJD2A uses the N-CoR complex to repress the ASCL2 gene, requiring both the JMJD2A tandem Tudor domain and a functional N-CoR complex. |
Co-immunoprecipitation, GST pull-down, ChIP cloning, siRNA knockdown, reporter assays |
Molecular and cellular biology |
Medium |
16024779
|
| 2004 |
The androgen receptor (AR) recruits endogenous NCoR to repress DHT-liganded AR target genes; mifepristone (RU486)-liganded AR markedly enhances the AR-NCoR interaction through the two most C-terminal nuclear receptor interacting domains of NCoR; this interaction requires both the AR ligand binding domain and the AR N-terminus via a surface distinct from the FXXLF motif. |
siRNA knockdown, chromatin immunoprecipitation, co-immunoprecipitation, mutagenesis |
The Journal of biological chemistry |
High |
15598662
|
| 2004 |
SMRT and N-CoR are regulated by distinct kinase signaling pathways: MEKK1 activation leads to phosphorylation of SMRT, its dissociation from transcription factors, and redistribution from nucleus to cytoplasm, whereas N-CoR is refractory to all these forms of MAPK regulation. |
In vitro and in vivo kinase assays, co-immunoprecipitation, subcellular fractionation/immunofluorescence |
The Journal of biological chemistry |
Medium |
15491994
|
| 2004 |
Unliganded TR recruits N-CoR/SMRT-TBLR1 complexes to chromatinized target promoters in vivo in Xenopus oocytes, accompanied by histone deacetylation and gene repression; dissociation of these complexes from TR target promoters during spontaneous Xenopus metamorphosis correlates with gene activation. |
Chromatin immunoprecipitation in Xenopus oocytes and tadpoles, dominant-negative N-CoR expression |
Molecular and cellular biology |
High |
15060155
|
| 2005 |
Rev-erbalpha represses the Bmal1 gene promoter by recruiting the endogenous N-CoR/HDAC3 complex via two monomeric Rev-erb binding sites, associated with decreased histone acetylation; reduction of HDAC3 markedly increases Bmal1 mRNA, establishing the N-CoR/HDAC3 complex as a corepressor for Rev-erbalpha in circadian rhythm regulation. |
ChIP, siRNA knockdown, reporter assays |
Molecular endocrinology |
High |
15761026
|
| 2005 |
Estrogen markedly down-regulates N-CoR protein levels (without affecting mRNA) in ER-positive breast cancer cells by upregulating the ubiquitin ligase Siah2, which targets N-CoR for proteasomal degradation; proteasomal inhibitors or Siah2 siRNA prevent N-CoR down-regulation by estrogen. |
Western blotting, siRNA knockdown of Siah2, proteasomal inhibitor treatment, reporter assays |
Proceedings of the National Academy of Sciences of the United States of America |
High |
16141343
|
| 2006 |
N-CoR is SUMOylated at K152, K1117, and K1330 by SUMO-E2 enzyme Ubc9 (which interacts with the N-CoR SANT1 domain) and SUMO-E3 ligase Pias1; SUMOylation at these sites within repression domains I and III contributes to transcriptional repression, as mutation of K152 in RD1 significantly reduces repression and abolishes the effect of Ubc9 on repression. |
In vitro SUMOylation assay, co-immunoprecipitation, site-directed mutagenesis, reporter assays |
Molecular biology of the cell |
Medium |
16421255
|
| 2006 |
The N-CoR complex enables chromatin remodeler SNF2H to enhance repression by unliganded TR; N-CoR and HDAC3 are both required for SNF2H recruitment to repressed TR target genes; SNF2H does not interact directly with N-CoR/HDAC3 but binds unacetylated histone H4 tails, suggesting HDAC3 deacetylase activity is critical for SNF2H function; SNF2H and HDAC3 are required for nucleosomal organization at TR target genes. |
ChIP on stably integrated reporter, siRNA knockdown, ChIP on endogenous gene |
The EMBO journal |
High |
16917504
|
| 2007 |
The AML1/ETO MYND domain binds SMRT and N-CoR; the solution structure of the MYND domain and an MYND-SMRT peptide complex was solved; a single amino acid substitution disrupting MYND-SMRT/N-CoR interaction attenuated AML1/ETO's effects on proliferation, differentiation, and gene expression of primary bone marrow cells. |
NMR structure determination, site-directed mutagenesis, primary cell functional assays |
Cancer cell |
High |
17560331
|
| 2007 |
N-CoR nuclear localization is a feature of undifferentiated glioblastoma stem-like cells; agents promoting N-CoR phosphorylation trigger its cytoplasmic translocation and astroglial differentiation in these cells. Treatment with retinoic acid and okadaic acid (which promotes phosphorylation) has synergistic growth inhibitory effects on glioma cell lines. |
Immunofluorescence localization, pharmacological phosphorylation induction, growth inhibition assays |
Cell cycle |
Medium |
17312396
|
| 2010 |
Crystal structure of Rev-erbalpha ligand-binding domain bound to an N-CoR interaction domain 1 (ID1) peptide reveals an unprecedented antiparallel beta-sheet interaction plus an alpha-helix out of register by four residues compared to ID2 structures; heme and ID1 peptide induce substantially different LBD conformational changes, suggesting Rev-erbalpha can mediate repression via ID1 binding independently of heme. |
X-ray crystallography, structural comparison |
Nature structural & molecular biology |
High |
20581824
|
| 2010 |
ERs recruit SMRT and N-CoR through an unusual mode involving multiple contact surfaces; the corepressor N-terminus contacts the receptor DNA binding domain (rather than the hormone binding domain), and this interaction is modulated by ER recognition of cognate DNA binding sites; several other nuclear receptors and N-CoR share this novel mode of corepressor recruitment. |
In vitro binding assays, mammalian two-hybrid, transcriptional reporter assays, domain mutagenesis |
Molecular and cellular biology |
Medium |
20065040
|
| 2011 |
Muscle-specific loss of NCoR1 in mice leads to enhanced exercise endurance due to increased muscle mass and mitochondrial number and activity, mediated by activation of transcription factors MEF2, PPARβ/δ, and ERRs; NCoR1 levels are decreased in conditions requiring fat oxidation; knockdown of gei-8 (the sole C. elegans NCoR1 homolog) also increases muscle mitochondria and respiration. |
Conditional knockout mice, exercise physiology, gene expression analysis, C. elegans RNAi knockdown |
Cell |
High |
22078881
|
| 2011 |
In vivo, NCoR1 is the principal mediator of thyroid hormone (TH) sensitivity: mice expressing the NCoR1ΔID allele (which cannot interact with TR or TRβ mutants) showed modest but significant correction of elevated TSH, TH levels, and thyroid hyperplasia in the RTH model (ThrβPV mice), demonstrating that aberrant NCoR1 recruitment by TRβ mutants contributes to clinical resistance to thyroid hormone. |
Genetic mouse models (ThrβPV × Ncor1ΔID crosses), thyroid function tests, tissue analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
21987803
|
| 2012 |
NCoR1 in skeletal muscle specifically antagonizes PGC-1α-mediated coactivation of ERRα to repress oxidative phosphorylation gene expression; NCoR1 and PGC-1α have opposing effects on the transcriptional activity of PPARβ/δ and ERRα. |
Muscle-specific knockout mice, gene expression analysis, transcriptional reporter assays with NCoR1 and PGC-1α co-expression |
Molecular and cellular biology |
High |
23028049
|
| 2013 |
Glucocorticoid-induced repression of the glucocorticoid receptor (GR) gene is mediated by recruitment of agonist-bound GR to an nGRE in exon 6, followed by assembly of a GR-NCoR1-HDAC3 repression complex at the transcription start site via a long-range chromatin interaction. |
ChIP, chromatin conformation capture (3C), siRNA knockdown, reporter assays |
Molecular and cellular biology |
High |
23428870
|
| 2013 |
In the liver, NCoR1 is the principal regulator of TH action in vivo; liver-specific deletion of NCoR1 (but not SMRT) markedly affects TH-regulated gene expression in both euthyroid and hypothyroid animals; combined deletion of NCoR1 and SMRT greatly accentuates hepatic lipid synthesis, indicating cooperativity in regulating multiple nuclear receptors including TR. |
Liver-specific conditional knockout mice, gene expression analysis, thyroid function tests |
Molecular and cellular biology |
High |
25421714
|
| 2013 |
TRα1PV mutant-mediated dominant negative activity in vivo depends on aberrant NCoR1 recruitment; crossing ThrαPV mice with NCoR1ΔID mice (which cannot recruit TRα1PV) partially reversed growth retardation, infertility, delayed bone development, and impaired adipogenesis through de-repression of PPARγ and C/EBPα. |
Genetic mouse crosses, growth and developmental phenotyping, gene expression analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
23610395
|
| 2015 |
SUMOylation of GR at K293 (human; K310 in mouse) within the N-terminal domain is mandatory for formation of a GR-SUMO-NCoR1/SMRT-HDAC3 repressing complex required for GC-induced IR nGRE-mediated direct transrepression in vitro; in keratinocyte-specific NCoR1/SMRT or HDAC3 knockout mice, Dex-induced direct repression and repressing complex formation on IR nGREs were impaired; HDAC3 binding to IR nGREs is mediated through interaction with SMRT/NCoR1. |
In vitro complex assembly, GR K310R mutant mice, skin keratinocyte-specific conditional knockout mice, ChIP |
Proceedings of the National Academy of Sciences of the United States of America |
High |
26712002 26712006
|
| 2016 |
NCOR1 and NCOR2 (SMRT) redundantly mediate RA-dependent repression of Fgf8 during somitogenesis; Ncor1;Ncor2 double mutants generated by CRISPR/Cas9 show increased Fgf8 expression and FGF signaling; embryo ChIP shows NCOR1/2 (but not coactivators) are recruited to the Fgf8 RARE in an RA-dependent manner, whereas coactivators (not NCOR1/2) are recruited to a RARE that activates Rarb. |
CRISPR/Cas9 double knockout mice, embryo ChIP, quantitative gene expression analysis |
Developmental biology |
High |
27506116
|
| 2016 |
USP44 is an integral subunit of the N-CoR complex; USP44 within N-CoR deubiquitinates histone H2B in vitro and in vivo; ablation of USP44 impairs N-CoR repressive activity; ChIP shows USP44 recruitment reduces H2Bub1 levels at N-CoR target loci. |
Co-purification/mass spectrometry, in vitro deubiquitination assay, ChIP, siRNA knockdown |
Cell reports |
High |
27880911
|
| 2016 |
MeCP2 anchors the NCoR1/HDAC3 repressor complex to lipogenesis target genes in hepatocytes; liver-targeted deletion of Mecp2 causes fatty liver disease and dyslipidemia similar to HDAC3 liver-specific deletion, demonstrating that MeCP2 is a component directing NCoR1/HDAC3 to specific genomic loci. |
Liver-specific conditional knockout mice, ChIP, gene expression analysis |
Human molecular genetics |
Medium |
27288453
|
| 2016 |
Loss of ULK1 increases RPS6KB1 signaling, which induces NCOR1 nuclear uptake, interaction with LXR/NR1H, and recruitment to the Scd1 promoter, thereby abrogating LXR-mediated Scd1 induction and increasing lipotoxicity in hepatic cells. |
siRNA knockdown, ChIP, co-immunoprecipitation, pharmacological inhibitors |
Autophagy |
Medium |
27846372
|
| 2018 |
NCoR1 is a critical scaffold component of the DRED repressor complex that recruits DNMT1 and LSD1 to γ-globin and ε-globin promoters via orphan nuclear receptors TR2/TR4; BAP1 deubiquitinase activity maintains NCoR1 at sites in the β-globin locus, and BAP1 inhibition massively induces γ-globin synthesis. |
Co-immunoprecipitation, ChIP, BAP1 inhibition studies, gene expression analysis |
Genes & development |
Medium |
30463901
|
| 2019 |
NCoR1 is degraded by selective autophagy through binding to GABARAP family autophagosomal proteins; loss of autophagy (Atg7 or Atg5 deletion) causes NCoR1 accumulation, which suppresses PPARα transactivation and impairs β-oxidation and ketone body production during fasting. |
Conditional knockout mice, co-immunoprecipitation with GABARAP proteins, gene expression analysis, metabolic assays |
Nature communications |
High |
30952864
|
| 2019 |
RNF20, a RING finger E3 ubiquitin ligase, promotes proteasomal degradation of NCoR1, thereby stimulating PPARγ transcriptional activity and adipogenesis; Rnf20-deficient mice exhibit reduced fat mass and smaller adipocytes. |
Conditional knockout mice, quantitative proteomics, co-immunoprecipitation, proteasomal degradation assays |
Diabetes |
Medium |
31604693
|
| 2019 |
Loss of NCOR1 and NCOR2 specifically in GABAergic neurons causes memory deficits associated with reduced GABRA2 expression in lateral hypothalamus GABAergic neurons, LHGABA neuron hyperexcitability, and impaired hippocampal LTP through a monosynaptic LHGABA→CA3GABA projection; this requires the NCOR1/2 deacetylase activation domain (DAD) for HDAC3 activation. |
GABAergic neuron-specific conditional knockout, optogenetics, electrophysiology, behavioral testing, de novo variant analysis in patients |
Nature neuroscience |
High |
30664766
|
| 2020 |
Myeloid cell-specific deletion of NCOR1 aggravates atherosclerosis; macrophage NCOR1 blocks pro-atherogenic PPARγ target genes (including CD36) in mouse and human macrophages, and NCOR1 deficiency increases CD36-mediated oxidized LDL uptake and foam cell formation. |
Myeloid-specific conditional knockout mice crossed with Ldlr knockout atherosclerosis model, gene expression analysis, foam cell assays |
European heart journal |
High |
31529020
|
| 2017 |
Many genomic changes mediated by unliganded TR in hypothyroidism (>43% of positive T3 targets) are independent of NCoR1; hypothyroidism-associated decreases in H3K27 acetylation at TRβ1-binding sites occur even in the absence of NCoR1, requiring TRβ1 but not NCoR1. |
Liver-specific NCoR1 knockout in hypothyroid mice, genome-wide H3K27 acetylation (ChIP-seq), liver-specific TRβ1 knockout |
Proceedings of the National Academy of Sciences of the United States of America |
High |
28923959
|