Affinage

BTG1

Protein BTG1 · UniProt P62324

Round 2 corrected
Length
171 aa
Mass
19.2 kDa
Annotated
2026-04-28
115 papers in source corpus 33 papers cited in narrative 33 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BTG1 is an antiproliferative transcriptional cofactor and mRNA decay regulator that enforces cellular quiescence and controls differentiation across multiple lineages. It exerts its functions through two principal biochemical axes: interaction with PRMT1 via its Box C motif to modulate arginine methylation of substrates such as ATF4 (Arg-239) and to coactivate nuclear receptors (GR, ERα, T3R, RAR) and myogenic factors, thereby linking cell cycle arrest to transcriptional programs in erythroid, B cell, hepatic, and muscle differentiation contexts (PMID:8663146, PMID:15674337, PMID:20354172, PMID:26657730); and interaction with the CAF1/CCR4-NOT deadenylase complex (via Box A/B domains) and PABPC1 (via Box C), promoting mRNA deadenylation and decay that maintains quiescence — most clearly demonstrated by globally increased mRNA stability and spontaneous T cell activation in BTG1/2 double-knockout T cells (PMID:32165587, PMID:34060423). Loss-of-function BTG1 mutations recurrent in diffuse large B cell lymphoma disrupt the α2–α4 binding interface required for CAF1/CNOT7/CNOT8 engagement, abolishing antiproliferative activity and converting germinal center B cells into supercompetitors with altered MYC induction kinetics that drive aggressive lymphomagenesis (PMID:33021411, PMID:36656933). In vivo, Btg1 deletion causes hyperproliferation followed by stem/progenitor depletion in adult neural niches, increased cardiomyocyte mitosis postnatally, and homeotic skeletal transformations consistent with Hox cofactor function (PMID:22969701, PMID:26524254, PMID:26218146).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1992 Medium

    The initial discovery that BTG1 overexpression inhibits NIH3T3 proliferation and that its expression peaks in G0/G1 established BTG1 as an antiproliferative gene linked to cell cycle exit.

    Evidence Transfection of NIH3T3 cells with BTG1 expression vector; Northern blot cell-cycle analysis

    PMID:1373383

    Open questions at the time
    • Mechanism of growth inhibition unknown
    • No binding partners identified
    • No in vivo validation
  2. 1996 High

    Identification of PRMT1 as a direct BTG1-interacting partner that modulates arginine methyltransferase activity revealed the first biochemical effector mechanism for BTG1's cellular functions.

    Evidence Yeast two-hybrid screen; GST pulldown; in vitro methyltransferase activity assay

    PMID:8663146

    Open questions at the time
    • Substrates of PRMT1 methylation downstream of BTG1 unknown
    • In vivo relevance not yet tested
  3. 1998 High

    Discovery that BTG1 binds CAF1/CCR4-NOT complex components via Box B, with the interaction regulated by CDK2-mediated Ser-159 phosphorylation, established a second major effector axis and linked BTG1 to transcriptional/post-transcriptional regulation via the CCR4 complex.

    Evidence Yeast two-hybrid; GST pulldown; Co-IP; in vitro kinase assay with purified CDKs; phosphorylation-site mutagenesis

    PMID:9712883 PMID:9820826

    Open questions at the time
    • Whether CAF1 interaction mediates deadenylation not yet tested
    • Functional consequence of Ser-159 phosphorylation on cell proliferation unresolved
  4. 2000 High

    Demonstration that BTG1 enhances Hoxb9-mediated transcription by stabilizing Hoxb9 DNA binding expanded the gene's role to transcriptional coactivation beyond the PRMT1 axis, and predicted developmental phenotypes.

    Evidence Yeast two-hybrid; GST pulldown; transient transfection reporter assays; EMSA

    PMID:10617598

    Open questions at the time
    • In vivo Hox-dependent developmental role not demonstrated
    • Whether BTG1 coactivation is direct or through adaptor recruitment unclear
  5. 2001 High

    Identification of LXXLL nuclear receptor box motifs as required for ERα regulation and mapping of localization signals showed that BTG1 acts as a nuclear transcriptional coactivator of nuclear receptors and that its nuclear localization is essential for myogenic differentiation activity.

    Evidence Co-IP; mutagenesis of LXXLL motifs; luciferase reporter assays; β-galactosidase fusion localization assays; myoblast differentiation readouts

    PMID:11136725 PMID:11420681

    Open questions at the time
    • Whether ER regulation operates through PRMT1 or CAF1 arm unclear
    • Endogenous target genes of BTG1-nuclear receptor complexes not identified
  6. 2004 High

    Positioning BTG1 as a FoxO3a transcriptional target that requires its PRMT1-binding domain to block erythroid colony outgrowth placed the BTG1/PRMT1 axis within a defined upstream signaling hierarchy controlling hematopoietic progenitor proliferation.

    Evidence Promoter-reporter assays; retroviral overexpression in primary bone marrow cells; colony assays; pharmacological methyltransferase inhibition; domain deletion mutants

    PMID:14734530

    Open questions at the time
    • PRMT1 substrates mediating erythroid arrest not identified
    • Whether FoxO3a-BTG1-PRMT1 axis operates in other lineages untested
  7. 2005 High

    Direct binding of BTG1 to T3R, RAR, and avian MyoD via A box/C-terminal domains, with mutagenesis showing these interactions are required for both transcriptional activation and myogenic differentiation, consolidated BTG1's identity as a multi-nuclear-receptor coactivator.

    Evidence Co-IP in myoblasts; GST pulldown with in vitro-translated proteins; transcriptional reporter assays; domain deletion mutagenesis

    PMID:15674337

    Open questions at the time
    • Whether coactivation involves PRMT1-dependent chromatin modification at target genes unknown
    • Genome-wide targets in myogenesis not mapped
  8. 2007 High

    Demonstration that Box C-mediated PRMT1 binding is required for anti-IgM-induced G1 arrest in B lymphoma cells, confirmed by both siRNA and pharmacological inhibition, established PRMT1 as the essential effector of BTG1 growth arrest in B cells.

    Evidence Retroviral overexpression; flow cytometry; PRMT1 siRNA; AdOx inhibition; Box C mutagenesis; immunoprecipitation with anti-dimethylarginine antibody

    PMID:17466295

    Open questions at the time
    • Identity of the 36-kDa methylated substrate unknown
    • Whether the CAF1-binding arm also contributes to B cell growth arrest untested
  9. 2010 High

    BTG1 was shown to determine glucocorticoid sensitivity in ALL by recruiting PRMT1 to the GR promoter in a BTG1-dependent manner, enabling GR autoinduction — the first ChIP-based evidence placing the BTG1/PRMT1 complex at a defined chromatin locus.

    Evidence shRNA knockdown; GR expression rescue; ChIP of PRMT1 at GR promoter; luciferase reporter assays

    PMID:20354172

    Open questions at the time
    • Whether PRMT1-catalyzed histone methylation or non-histone substrate methylation mediates GR induction unclear
    • Clinical validation in ALL patients lacking
  10. 2012 High

    Btg1 knockout mice revealed that Btg1 is essential for maintaining adult neural stem cell quiescence: loss causes transient hyperproliferation followed by p53/p21-dependent apoptosis and progressive stem cell depletion, providing the first in vivo demonstration that Btg1 safeguards stem cell pools.

    Evidence Btg1 KO mice; BrdU/EdU incorporation; immunofluorescence for p53, p21, activated caspase-3; neurosphere self-renewal assay

    PMID:22969701

    Open questions at the time
    • Direct molecular targets of BTG1 in neural stem cells not identified
    • Whether PRMT1 or CAF1 arm mediates quiescence in this niche unknown
  11. 2015 High

    Multiple in vivo studies converged to show BTG1 controls cyclin D1-dependent cerebellar granule precursor proliferation, synergizes with BTG2 in Hox-dependent axial skeleton patterning, and modulates ATF4 methylation at Arg-239 to regulate stress adaptation — establishing BTG1 as a pleiotropic developmental and stress-response regulator acting through distinct molecular effectors.

    Evidence Btg1 and Btg1/Btg2 DKO mice; skeletal preparations; cyclin D1 readouts in GCP cell line; co-IP of BTG1-ATF4; in vitro methylation identifying Arg-239; stress survival assays in KO MEFs and B-cell progenitors

    PMID:26396236 PMID:26524254 PMID:26657730

    Open questions at the time
    • Whether cyclin D1 regulation is direct or indirect unclear
    • Structural basis for ATF4 methylation site selectivity unknown
  12. 2016 High

    BTG1 was placed within the mTOR/S6K1/CREB regulatory axis in hepatocytes, where it suppresses ATF4-driven SCD1 expression to prevent steatosis and improves insulin sensitivity via c-Jun upregulation, extending its antiproliferative cofactor role to metabolic homeostasis.

    Evidence Adenovirus-mediated overexpression/knockdown in vivo; BTG1 transgenic mice; ATF4 overexpression rescue; SCD1 knockdown epistasis; insulin and glucose tolerance tests

    PMID:26396236 PMID:27188441

    Open questions at the time
    • Whether the hepatic metabolic role requires PRMT1 enzymatic activity not directly tested
    • Human liver disease relevance not established
  13. 2020 High

    The deadenylation function of BTG1/2 was definitively established: double-knockout T cells showed globally lengthened poly(A) tails and increased mRNA half-lives causing spontaneous activation, while lymphoma-associated BTG1 mutations were shown to disrupt CNOT7/CNOT8 binding and abolish antiproliferative and mRNA decay activity.

    Evidence BTG1/2 DKO T cells; RNA-seq; poly(A) tail sequencing; mRNA half-life measurement; functional assays of 16 DLBCL BTG1 variants for CNOT7/CNOT8 binding and antiproliferative activity

    PMID:32165587 PMID:33021411

    Open questions at the time
    • Whether specific mRNA targets mediate the quiescence phenotype or the effect is global remains unclear
    • Relative contribution of PRMT1 versus CAF1/PABPC1 arms to BTG1 tumor suppression in lymphoma unresolved
  14. 2021 High

    NMR-based structural dissection showed the Box C motif is necessary and sufficient for PABPC1 interaction and stimulation of mRNA deadenylation, completing the molecular anatomy of the BTG1 deadenylation axis (Box A/B for CAF1, Box C for PABPC1).

    Evidence NMR spectroscopy; Box C mutational analysis; GST pulldown; co-IP; in vitro and cellular deadenylation assays

    PMID:34060423

    Open questions at the time
    • Full structure of BTG1-PABPC1-CAF1 ternary complex not determined
    • Whether PABPC1 binding is regulated by post-translational modification unknown
  15. 2023 High

    BTG1 mutations in germinal center B cells were shown to create supercompetitors via altered MYC induction kinetics, and BTG1 loss was found to activate a BCAR1-RAC1 migration pathway targetable by dasatinib, revealing two distinct pathogenic mechanisms in DLBCL.

    Evidence Mouse models of BTG1 mutation; competitive GC B cell assays; MYC induction kinetics; Co-IP of BTG1-BCAR1; RAC1 activation and migration assays; dasatinib treatment in vivo

    PMID:36375119 PMID:36656933

    Open questions at the time
    • Whether MYC kinetics shift is mediated through the deadenylation or PRMT1 arm not determined
    • Clinical efficacy of dasatinib in BTG1-mutant DLBCL unvalidated
    • BCAR1 interaction domain on BTG1 not mapped

Open questions

Synthesis pass · forward-looking unresolved questions
  • A unified quantitative model of how the PRMT1-dependent and CAF1/PABPC1-dependent arms of BTG1 are coordinately deployed in different cellular contexts — and which arm is dominant for tumor suppression in specific cancer types — remains unresolved.
  • No high-resolution structure of full-length BTG1 in complex with both PRMT1 and CAF1/PABPC1
  • Genome-wide identification of mRNA targets whose deadenylation is BTG1-dependent in normal versus malignant B cells lacking
  • Context-dependent relative contributions of PRMT1 and deadenylation arms to tumor suppression not dissected

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 6 GO:0060090 molecular adaptor activity 4 GO:0140110 transcription regulator activity 4
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1266738 Developmental Biology 3 R-HSA-168256 Immune System 3 R-HSA-5357801 Programmed Cell Death 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-1430728 Metabolism 2
Partners
ATF4BCAR1CNOT7CNOT8HOXB9NR3C1PABPC1PRMT1
Complex memberships
CCR4-NOT deadenylase complex

Evidence

Reading pass · 33 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 BTG1 was identified as an antiproliferative gene whose overexpression negatively regulates cell proliferation in NIH3T3 cells, and its expression is maximal in the G0/G1 phases of the cell cycle, decreasing as cells progress through G1. Transfection of NIH3T3 cells with BTG1 expression vector; Northern blot cell-cycle analysis The EMBO journal Medium 1373383
1996 BTG1 (and its paralog TIS21) physically interacts with PRMT1 (protein-arginine N-methyltransferase 1) via yeast two-hybrid, and GST-BTG1 fusion protein qualitatively and quantitatively modulates endogenous PRMT1 arginine methyltransferase activity in cell extracts, identifying PRMT1 as a functional effector of BTG1. Yeast two-hybrid screen; GST pulldown; in vitro methyltransferase activity assay with cell extracts The Journal of biological chemistry High 8663146
1998 BTG1 and BTG2 physically interact with mCaf1 (mouse CCR4-associated factor 1, a component of the yeast CCR4 transcriptional regulatory complex) both in vitro and in vivo in HeLa cells; the conserved Box B domain of BTG1 is essential for this interaction, suggesting BTG proteins participate in transcriptional regulation of cell-cycle genes via the CCR4-NOT complex. Yeast two-hybrid screening; GST pulldown (protein-binding assay); co-immunoprecipitation in HeLa cells; deletion mutagenesis of Box B The Journal of biological chemistry High 9712883
1998 BTG1 interaction with hCAF1 (human CCR4-associated factor 1) requires phosphorylation of Ser-159 on BTG1 by CDK2/cyclin E or CDK2/cyclin A (but not CDK4/cyclin D1 or CDC2/cyclin B); an Ala-159 mutant fails to interact with hCAF1 in yeast. In contact-inhibited smooth muscle cells, BTG1 and rCAF1 co-localize in the nucleus and co-immunoprecipitate. Yeast two-hybrid with phosphorylation-site mutants; in vitro kinase assay with purified CDKs; co-immunoprecipitation from cell extracts; immunohistochemistry; cell synchrony experiments The Biochemical journal High 9820826
2000 BTG1 and BTG2 physically interact with the homeodomain transcription factor Hoxb9 via yeast two-hybrid and in vitro binding, and enhance Hoxb9-mediated transcription in transfected cells; the Hoxb9·BTG2 complex forms on a Hoxb9-responsive DNA target, facilitating Hoxb9 DNA binding. The transcriptional activation is dependent on the N-terminal activation domain of Hoxb9. Yeast two-hybrid; GST pulldown; transient transfection transcription assays; electrophoretic mobility shift assay (EMSA) The Journal of biological chemistry High 10617598
2001 BTG1 and BTG2 interact with both hCAF1 and hPOP2 (human paralogs of the CCR4-associated factor). Two LXXLL nuclear receptor box motifs in BTG1 and BTG2 are required for regulation of estrogen receptor alpha (ERα)-mediated transcription; BTG proteins can act as both positive and negative regulators of ERα function, likely through a CCR4-like complex. Yeast two-hybrid; GST pulldown; co-immunoprecipitation; transient transfection luciferase transcription assays; deletion/mutagenesis of LXXLL motifs The Journal of biological chemistry High 11136725
2001 The subcellular localization of BTG1 is controlled by multiple domains: the conserved B box mediates nuclear localization, a functional Nuclear Export Signal (NES) overlaps the B box, the first 43 N-terminal amino acids reduce nuclear accumulation, an LxxLL motif favors nuclear accumulation, and the A box inhibits nuclear localization. A nuclear-localized BTG1 mutant enhances myoblast withdrawal from the cell cycle and terminal differentiation, whereas a cytoplasmic-only mutant does not, establishing that BTG1 myogenic activity operates from the nucleus. Beta-galactosidase fusion localization assays; domain deletion/mutation constructs; transient expression in myoblasts with cell cycle and differentiation readouts Oncogene Medium 11420681
2004 FoxO3a directly targets the BTG1 promoter and induces BTG1 expression during erythroid differentiation. BTG1 expression in primary mouse bone marrow cells blocks erythroid colony outgrowth, and this anti-proliferative effect requires the domain of BTG1 that binds PRMT1. Inhibition of methyltransferase activity blocks erythroid maturation, placing the BTG1/PRMT1 axis as a downstream effector of FoxO3a in controlling erythroid expansion. Promoter-reporter assays; retroviral overexpression in primary bone marrow cells; colony formation assay; pharmacological inhibition of methyltransferase; BTG1 domain deletion mutants The Journal of cell biology High 14734530
2004 BTG1 overexpression in cultured endothelial cells augments tube formation and cell migration on Matrigel, while antisense BTG1 inhibits network formation; BTG1 mRNA is up-regulated in tube-forming endothelial cells and by TGF-β, defining a pro-angiogenic role for BTG1 in this cellular context. Antisense and sense BTG1 overexpression in endothelial cells; Matrigel tube formation assay; cell migration assay; neutralizing antibody against TGF-β Biochemical and biophysical research communications Medium 15033446
2005 BTG1 directly interacts with thyroid hormone receptor (T3R) and all-trans retinoic acid receptor (RAR) (but not RXRα or PPARγ), and with the myogenic factor avian MyoD (CMD1), as shown by co-immunoprecipitation in cells and GST pulldown with in vitro-synthesized proteins. These interactions are mediated by the transactivation domain of each transcription factor and the A box plus C-terminal region of BTG1. Deletion of BTG1 interacting domains abolishes its ability to stimulate nuclear receptor and CMD1 activity and its myogenic influence, establishing BTG1 as a transcriptional coactivator during myoblast differentiation. Co-immunoprecipitation in cultured myoblasts; GST pulldown with in vitro-translated proteins; transcriptional reporter assays; BTG1 deletion mutagenesis; myoblast differentiation assays Oncogene High 15674337
2007 BTG1 and BTG2 bind PRMT1 via their Box C region; this interaction is required for anti-IgM-induced G1 growth arrest in WEHI-231 B lymphoma cells. Pharmacological inhibition of arginine methyltransferase (AdOx) or siRNA knockdown of PRMT1 abrogates BTG1/BTG2-induced growth inhibition. Anti-IgM stimulation induces PRMT1-dependent arginine methylation of a 36-kDa protein substrate within 1-2 hours. Retroviral overexpression; flow cytometry (cell cycle); pharmacological inhibition with AdOx; siRNA knockdown of PRMT1; immunoprecipitation with anti-asymmetric dimethylarginine antibody; BTG1 domain mutagenesis (Box C) Experimental cell research High 17466295
2010 BTG1 is a key determinant of glucocorticoid (GC) responsiveness in acute lymphoblastic leukemia: BTG1 knockdown causes GC resistance by reducing glucocorticoid receptor (GR) expression and impairing GR-mediated transcription, while BTG1 re-expression restores GC sensitivity by potentiating GC-induced GR autoinduction. PRMT1, a BTG1-binding partner, is recruited to the GR gene promoter in a BTG1-dependent manner, implicating the BTG1/PRMT1 complex as a transcriptional coactivator of GR. RNA interference (shRNA); GR expression rescue experiments; chromatin immunoprecipitation (ChIP) of PRMT1 at GR promoter; luciferase reporter assays Blood High 20354172
2012 Btg1 knockout mice show transient early hyperproliferation followed by progressive depletion of adult stem and progenitor cells in the dentate gyrus and subventricular zone. Adult Btg1-null stem/progenitor cells exit the cell cycle after S phase, upregulate p53 and p21, and undergo apoptosis within 5 days, indicating that Btg1 is required for maintaining adult neural stem cell quiescence and self-renewal. Btg1 knockout mouse generation; BrdU/EdU incorporation; immunofluorescence for p53, p21, activated caspase-3; neurosphere self-renewal assay; contextual memory behavioral tests Frontiers in neuroscience High 22969701
2015 Btg1 regulates cerebellar granule precursor (GCP) proliferation selectively through cyclin D1: Btg1 knockout causes increased GCP proliferation and EGL hyperplasia, while gain- and loss-of-function experiments in a GCP cell line confirm that Btg1 controls proliferation via cyclin D1. Combined Btg1/Tis21 double knockout reveals additive defects in proliferation and migration. Btg1-null mice display permanent increase in adult cerebellar volume and impaired motor coordination. Btg1 single and double (Btg1/Tis21) knockout mice; BrdU incorporation; immunohistochemistry; gain- and loss-of-function in GCP cell line with cyclin D1 readout; behavioral motor testing Developmental biology High 26524254
2015 BTG1 interacts with PRMT1 in renal cell carcinoma cells; BTG1 overexpression induces G0/G1 arrest and apoptosis in 786-O cells, and pharmacological blocking of PRMT1 activity inhibits BTG1 function, demonstrating that BTG1's anti-proliferative and pro-apoptotic effects in RCC require PRMT1 activity. Co-immunoprecipitation; BTG1 overexpression with flow cytometry (cell cycle, apoptosis); PRMT1 inhibitor treatment Oncology letters Medium 26622543
2016 BTG1 interacts with ATF4 and recruits PRMT1 to methylate ATF4 at arginine residue 239, positively modulating ATF4 transcriptional activity. Loss of Btg1 in MEFs provides a survival advantage under stress conditions (hypoxia, nutrient limitation) by altering ATF4-mediated stress responses. Loss of Btg1 also enhances stress adaptation of bone marrow-derived B-cell progenitors. Btg1 knockout MEFs and B-cell progenitors; co-immunoprecipitation of BTG1-ATF4; in vitro methylation assay identifying Arg-239 as PRMT1 target; cell survival assays under stress; luciferase reporter assays for ATF4 activity Oncotarget High 26657730
2016 BTG1 overexpression in db/db obese mice ameliorates liver steatosis, while BTG1 knockdown induces steatosis in wild-type mice. BTG1 suppresses ATF4 activity to inhibit SCD1 (stearoyl-CoA desaturase 1) gene expression, thereby reducing hepatic triglyceride accumulation. BTG1 expression itself is regulated by the mTOR/S6K1/CREB pathway. Adenovirus-mediated overexpression/knockdown in vivo; BTG1 transgenic mice on high-carbohydrate diet; ATF4 overexpression rescue; SCD1 knockdown epistasis; hepatic lipid quantification Science signaling High 27188441
2015 BTG1 regulates hepatic insulin sensitivity via upregulation of c-Jun expression: BTG1 overexpression improves insulin signaling in vitro and in vivo (db/db mice), while BTG1 knockdown impairs it. c-Jun knockdown blocks the BTG1-mediated improvement in insulin sensitivity. BTG1 promotes c-Jun expression by stimulating c-Jun and retinoic acid receptor transcriptional activities. Hepatic BTG1 is increased by leucine deprivation through the mTOR/S6K1 pathway. Adenovirus-mediated BTG1 overexpression/knockdown in vivo and in vitro; BTG1 transgenic mice; insulin tolerance and glucose tolerance tests; c-Jun knockdown epistasis; luciferase reporter assays FASEB journal High 26396236
2020 BTG1 and BTG2 promote mRNA deadenylation and decay to maintain T cell quiescence. BTG1/2-deficient T cells show globally increased mRNA abundance due to lengthened poly(A) tails and greater mRNA half-life, reducing the activation threshold and causing spontaneous T cell activation and proliferation. BTG1/2 thus function as regulators of the deadenylation machinery to control quiescence. BTG1/BTG2 double-knockout T cells; RNA-seq; poly(A) tail length sequencing; mRNA half-life measurement; T cell activation and proliferation assays Science (New York, N.Y.) High 32165587
2021 The Box C motif in BTG1 (and BTG2) is necessary and sufficient for interaction with the first RRM domain of cytoplasmic poly(A) binding protein PABPC1, and this interaction—demonstrated by NMR and mutagenesis—endows the APRO domain with the ability to stimulate mRNA deadenylation both in cellulo and in vitro. Unexpectedly, Box C is not required for BTG2 interaction with PRMT1. NMR spectroscopy; mutational analysis (Box C deletions/mutations); GST pulldown and co-immunoprecipitation; in vitro and cellular deadenylation assays RNA biology High 34060423
2020 Disease-associated BTG1 mutations found in non-Hodgkin lymphoma impair interaction with CNOT7 and CNOT8 (the Caf1 catalytic subunit of the CCR4-NOT deadenylase complex) and reduce BTG1 anti-proliferative activity, cell cycle inhibition, translational repression, and mRNA degradation activity, establishing loss of CCR4-NOT engagement as a mechanism of BTG1 inactivation in lymphoma. In silico selection of 16 BTG1 variants; protein-protein interaction assays with CNOT7/CNOT8; cell cycle assays; translational repression assays; mRNA degradation assays Leukemia & lymphoma Medium 33021411
2023 BTG1 mutations in germinal center B cells disrupt a gatekeeper mechanism limiting B cell fitness during affinity maturation, converting GC B cells into 'supercompetitors' that outstrip wild-type counterparts. This competitive advantage is conferred by a small shift in MYC protein induction kinetics and leads to aggressive invasive lymphomas. BTG1 mutations are enriched in MCD/C5 DLBCL subtype. Primary human lymphoma genomics; new mouse models of BTG1 mutation; competitive GC B cell assays; MYC induction kinetics measurement; in vivo lymphoma models Science (New York, N.Y.) High 36656933
2023 BTG1 inactivation accelerates lymphoproliferative disease driven by BCL2 overexpression. BTG1 directly interacts with the scaffolding protein BCAR1, and BTG1 deletion or DLBCL-associated BTG1 mutations cause overactivation of the BCAR1-RAC1 pathway, conferring increased B cell migration ability in vitro and in vivo. This is targetable with the SRC inhibitor dasatinib. Btg1 knockout mouse crossed onto Bcl2-overexpressing background; co-immunoprecipitation (BTG1-BCAR1); RAC1 activation assay; in vitro migration assays; in vivo dissemination models; dasatinib treatment Blood High 36375119
2022 Molecular dynamics simulations reveal that the α2-α4 interface of BTG1 undergoes conformational transitions between 'closed' and 'open' metastable states, and this interface serves as a binding hotspot for cellular partners. DLBCL mutations (Q36H, F40C, Q45P, E50K in α2; A83T, A84E in α4) either overstabilize one state or distort the helices, disrupting the dynamic equilibrium required for productive interactions with binding partners. Atomistic molecular dynamics simulations; Markov state modeling; structural analysis of WT and DLBCL mutants Biophysical journal Low 35459639
2023 Btg1 and Btg2 contribute to postnatal cardiomyocyte cell cycle arrest: double knockout (DKO) mice show increased mitotic cardiomyocytes at postnatal day 7 but not day 30. AAV9-mediated double knockdown confirms increased EdU+ cardiomyocytes at P7. siRNA-mediated knockdown in neonatal rat ventricular myocytes increases EdU+ cardiomyocytes without binucleation or ploidy increase. RNAseq supports roles in inhibiting proliferation and modulating ROS response pathways. Btg1/2 double knockout mice; AAV9-shRNA knockdown; siRNA knockdown in NRVMs; EdU/pHH3 incorporation assays; RNAseq Journal of molecular and cellular cardiology Medium 37062247
2015 Targeted deletion of Btg1 and Btg2 causes homeotic transformation of the axial skeleton (posterior transformation of cervical, thoracic, and lumbar vertebrae), with Btg1 and Btg2 acting synergistically. These phenotypes are consistent with roles as modulators of Hox transcription factor function in vivo. Btg1 single KO, Btg2 single KO, and Btg1/Btg2 double KO mice; skeletal preparation and analysis of vertebral identity PloS one Medium 26218146
2015 BTG1 expression in developing limb digit blastemas negatively influences cartilage differentiation in micromass cultures, accompanied by upregulation of Ccn1, Scleraxis, and PTHrP. BTG1 overexpression upregulates retinoic acid and thyroid hormone receptors but its connective tissue differentiation influence appears independent of these nuclear receptor signaling pathways in this context. In situ hybridization in developing limb; gain- and loss-of-function in micromass cultures; qRT-PCR for target genes Cell and tissue research Low 26662056
2021 Chidamide (HDAC inhibitor) identifies BTG1 as a target gene in resistant B-cell lymphoma: ChIP analysis shows BTG1 is epigenetically regulated by histone deacetylase activity. BTG1 controls autophagy in rituximab/chemotherapy-resistant lymphoma cells, contributing to chidamide-induced cell death. RNA-seq; chromatin immunoprecipitation (ChIP); autophagy assays; cell death assays in resistant lymphoma cells and mouse xenograft model Cell death & disease Medium 34599153
2026 BTG1 is epigenetically upregulated by HDAC inhibition in DLBCL cells and suppresses β-catenin signaling by inhibiting formation of the β-catenin/TCF4 transcriptional complex, reducing downstream targets c-Myc and Cyclin D1. BTG1 is necessary and sufficient for HDAC inhibitor-induced cell cycle arrest and autophagy in DLBCL. In vivo antitumor efficacy of HDAC inhibition depends on the BTG1/β-catenin axis. BTG1 overexpression and siRNA knockdown; co-immunoprecipitation of β-catenin/TCF4 complex; luciferase reporter for β-catenin/TCF4 activity; DLBCL xenograft mouse model; cell cycle and autophagy assays Molecular carcinogenesis Medium 41950351
2020 Loss of Btg1 in medulloblastoma (Ptch1+/- background) increases apoptosis of neoplastic cerebellar granule precursors (marked by activated caspase-3) and is associated with increased PRMT1 protein expression. Pro-apoptotic gene BAD is a PRMT1 target, suggesting increased PRMT1 activity mediates the apoptosis increase in Btg1-null tumors. Btg1 ablation also doubles CD15+ tumor stem cells in medulloblastoma. Btg1/Ptch1 double mutant mice; immunostaining for activated caspase-3 and PRMT1; CD15 staining for tumor stem cells; analysis of BAD as PRMT1 target Frontiers in oncology Medium 32231994
2018 BTG1 deficiency enhances the self-renewal of ETV6-RUNX1-positive fetal liver hematopoietic progenitors, and combined ETV6-RUNX1 expression with BTG1 loss drives upregulation of BCL6 and suppression of its targets p19Arf and Tp53. BTG1 thus limits BCL6 expression downstream of ETV6-RUNX1, acting as a tumor suppressor by restraining a BCL6-driven self-renewal program. Btg1-deficient mouse fetal liver hematopoietic progenitors; ETV6-RUNX1 retroviral expression; serial replating/self-renewal assays; gene expression analysis of BCL6, p19Arf, Tp53; ectopic BCL6 expression rescue Experimental hematology Medium 29408281
1999 BTG1 overexpression in quail myoblasts mimics triiodothyronine (T3) and cAMP myogenic influences: it inhibits myoblast proliferation by increasing cell cycle withdrawal and stimulates terminal differentiation. T3 and cAMP stimulate BTG1 nuclear accumulation in confluent myoblasts. AP-1 activity represses BTG1 expression via an AP-1-like sequence in the BTG1 promoter, explaining low BTG1 levels in proliferating cells. Transient transfection and stable overexpression in quail myoblasts; cell cycle analysis; differentiation assays; promoter-reporter assays with AP-1 site mutation; subcellular localization by immunofluorescence Experimental cell research Medium 10366433
2019 PUM2 (an RNA-binding protein) binds directly to the BTG1 3'UTR as demonstrated by RNA pulldown and RNA immunoprecipitation, repressing BTG1 expression at the post-transcriptional level. PUM2 knockdown in glioblastoma cells suppresses proliferation and migration, and these effects are reversed by BTG1 knockdown, placing BTG1 as a functional downstream target of PUM2-mediated post-transcriptional repression. RNA pulldown assay; RNA immunoprecipitation (RIP); shRNA knockdown of PUM2 and BTG1; CCK-8 proliferation assay; migration/invasion assay Cell structure and function Medium 30787206

Source papers

Stage 0 corpus · 115 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
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
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2003 Exploring proteomes and analyzing protein processing by mass spectrometric identification of sorted N-terminal peptides. Nature biotechnology 485 12665801
1979 Platelet alpha-granule proteins: studies on release and subcellular localization. Blood 464 426909
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
1996 The mammalian immediate-early TIS21 protein and the leukemia-associated BTG1 protein interact with a protein-arginine N-methyltransferase. The Journal of biological chemistry 416 8663146
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1996 The CXC chemokines growth-regulated oncogene (GRO) alpha, GRObeta, GROgamma, neutrophil-activating peptide-2, and epithelial cell-derived neutrophil-activating peptide-78 are potent agonists for the type B, but not the type A, human interleukin-8 receptor. The Journal of biological chemistry 354 8702798
1992 BTG1, a member of a new family of antiproliferative genes. The EMBO journal 276 1373383
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