| 1998 |
HRMT1L2 (human PRMT1) encodes a protein arginine methyltransferase that exhibits methyltransferase activity in vitro and can complement a yeast HMT1 mutant strain in vivo, establishing it as the human ortholog of yeast Hmt1p. |
In vitro methyltransferase assay with recombinant protein; yeast complementation assay |
Genomics |
High |
9545638
|
| 2015 |
PRMT1 methylates RBM15 at R578, leading to its ubiquitylation by the E3 ligase CNOT4 and subsequent proteasomal degradation; this reduces RBM15 protein levels and alters alternative splicing of megakaryocytic genes (GATA1, RUNX1, TAL1, c-MPL) by displacing the splicing factor SF3B1 from intronic regions. |
Co-IP, in vitro methylation assay, mass spectrometry, RNA-seq, ChIP, overexpression/knockdown in leukemia cell lines |
eLife |
High |
26575292
|
| 2015 |
PRMT1 methylates EGFR at R198 and R200 in the extracellular domain, enhancing EGF binding, receptor dimerization, and downstream signaling activation; methylation-defective EGFR reduces tumor growth in orthotopic models and increased methylation confers resistance to cetuximab. |
In vitro methylation assay, site-directed mutagenesis, mouse xenograft model, mass spectrometry |
The Journal of clinical investigation |
High |
26571401
|
| 2015 |
PRMT1 enzymatic activity is regulated by oxidation: H2O2 oxidizes one or more cysteine residues of PRMT1 to sulfenic acid, impairing methyltransferase activity in a concentration-dependent and reversible manner. |
In vitro methyltransferase activity assay, chemical modification with H2O2, reduction rescue experiments |
The Journal of biological chemistry |
High |
25911106
|
| 2017 |
PRMT1 methylates CDK4, preventing formation of the CDK4–Cyclin-D3 complex and thereby inducing cell cycle arrest in pre-B cells; BTG2 acts together with PRMT1 in this module to limit pre-B cell expansion and suppress leukemogenesis. |
Co-IP, in vitro methylation assay, cell cycle analysis, in vivo pre-B cell leukemia model |
Nature immunology |
High |
28628091
|
| 2018 |
PRMT1 interacts with and methylates CaMKII at R9 and R275, leading to inhibition of CaMKII activity; cardiac-specific PRMT1 ablation causes CaMKII hyperactivation, dilated cardiomyopathy, and heart failure, rescued by pharmacological CaMKII inhibition. |
Cardiac-specific knockout mice, Co-IP, in vitro methylation assay, site-directed mutagenesis, pharmacological rescue |
Nature communications |
High |
30504773
|
| 2018 |
PRMT1 facilitates TGF-β signaling by methylating SMAD7 at the TGF-β receptor complex, promoting SMAD7 dissociation from the receptor and enabling SMAD3 activation, thereby driving epithelial-to-mesenchymal transition and epithelial stem-cell generation. |
In vitro methylation assay, Co-IP, PRMT1 depletion with functional EMT readouts, receptor complex analysis |
The Journal of biological chemistry |
High |
29907569
|
| 2018 |
GFI1 interacts with PRMT1 and enables PRMT1 to bind and methylate MRE11 and 53BP1, modifications required for their function in the DNA damage response; GFI1 deletion causes hypersensitivity to ionizing radiation due to impaired PRMT1-mediated methylation of these repair proteins. |
Co-IP, in vitro methylation assay, GFI1 knockout cells, ionizing radiation sensitivity assay |
Nature communications |
High |
29651020
|
| 2017 |
PRMT1 methylates the RGG motif of UBAP2L, and increased arginine methylation of UBAP2L blocks its interaction with stress granule (SG) components, while decreased methylation promotes SG assembly; UBAP2L is thus regulated by PRMT1 to control stress granule dynamics. |
Co-IP, in vitro methylation assay, live-cell imaging, overexpression/knockdown of PRMT1 and UBAP2L |
Cell death and differentiation |
High |
31114027
|
| 2019 |
Skeletal muscle-specific PRMT1 deletion causes muscle atrophy; in the absence of PRMT1, PRMT6 levels increase and specifically methylates FOXO3 at R188 and R249, activating FOXO3 and upregulating atrogenes TRIM63 and FBXO32; PRMT6 depletion abrogates FOXO3 hyperactivation in PRMT1-deficient muscle. |
Conditional knockout mice, adenoviral shRNA, in vitro methylation assay, epistasis (PRMT6 depletion rescue) |
Autophagy |
High |
30653406
|
| 2017 |
PRMT1 methylates the co-activator Eya1; loss of PRMT1 in muscle stem cells prevents Eya1 methylation and reduces its recruitment to the MyoD promoter, impairing MyoD expression and blocking myogenic differentiation. |
Pax7CreERT2 conditional PRMT1 KO, in vitro methylation assay, ChIP, muscle regeneration assay |
Molecular and cellular biology |
High |
27849571
|
| 2017 |
CSNK1a1 kinase directly phosphorylates PRMT1, controlling PRMT1 genomic targeting to proliferation genes and differentiation-suppressing genes (including GRHL3); this cooperation between CSNK1a1 and PRMT1 maintains epidermal progenitor self-renewal. |
Mass spectrometry interactome, Co-IP, kinase assay, mouse knockout, ChIP-seq, mosaic human epidermis regeneration |
Developmental cell |
High |
28943242
|
| 2017 |
TRIM48 promotes K48-linked polyubiquitination and degradation of PRMT1; PRMT1 negatively regulates ASK1 by enhancing its interaction with thioredoxin (Trx); thus TRIM48 activates ASK1 by relieving PRMT1-mediated suppression. |
Pulldown screen, Co-IP, ubiquitination assay, ASK1 kinase assay, TRIM48 knockdown/overexpression |
Cell reports |
High |
29186683
|
| 2020 |
DNA-PK binds to and phosphorylates PRMT1 in response to cisplatin, inducing PRMT1 chromatin recruitment and redirecting its enzymatic activity to deposit H4R3me2a at pro-inflammatory gene promoters, driving the senescence-associated secretory phenotype. |
MS-based proteomics, Co-IP, ChIP, kinase assay, cisplatin treatment |
Cell reports |
High |
31995759
|
| 2021 |
PRMT1-mediated H4R3me2a histone mark directly recruits SMARCA4 (an ATPase subunit of the SWI/SNF complex) to promote transcription of EGFR and TNS4, enhancing colorectal cancer proliferation and migration. |
Co-IP, ChIP-seq, biochemical histone binding assay, cell viability/migration assays, in vivo CRC mouse model |
Genome medicine |
High |
33853662
|
| 2021 |
PRMT1 promotes TBK1 activation by catalyzing asymmetric dimethylation of R54, R134, and R228 on TBK1, which enhances TBK1 oligomerization after viral infection and promotes downstream type I interferon production; myeloid-specific Prmt1 KO mice are more susceptible to viral infection. |
In vitro methylation assay, Co-IP, TBK1 oligomerization assay, myeloid-specific KO mice, viral challenge |
Cell reports |
High |
34551290
|
| 2020 |
PRMT1 asymmetrically dimethylates EZH2 at R342 (meR342-EZH2), which inhibits CDK1-mediated phosphorylation of EZH2 at T345 and T487, thereby attenuating TRAF6-mediated EZH2 ubiquitylation and increasing EZH2 stability to promote breast cancer EMT and metastasis. |
In vitro methylation assay, site-directed mutagenesis, Co-IP, ubiquitination assay, in vivo xenograft |
Cell death and differentiation |
High |
32895488
|
| 2019 |
PRMT1 methylates C/EBPα at R35, R156, and R165; this methylation blocks the interaction of C/EBPα with its corepressor HDAC3, promoting cyclin D1 expression and breast cancer cell proliferation. |
Tandem affinity purification/mass spectrometry, Co-IP, in vitro methylation, site-directed mutagenesis, RNA-seq |
Cancer research |
High |
31015230
|
| 2019 |
PRMT1 constitutively associates with IGF-1R and becomes activated upon IGF-1 stimulation; activated PRMT1 methylates ERα at R260, inducing formation of the mERα/Src/PI3K complex and propagating non-genomic IGF-1 signaling in breast cancer cells. |
Co-IP, in vitro methylation assay, PRMT1 inhibition (pharmacological and knockdown), signaling assays |
Oncogene |
High |
30692633
|
| 2019 |
PRMT1 methylates SMAD7 arginine residues at the TGF-β receptor complex, promoting SMAD7 dissociation and enabling SMAD3-mediated downstream signaling; similar mechanism operates for BMP-induced SMAD6 methylation. |
In vitro methylation assay, receptor complex Co-IP, PRMT1 knockdown, EMT functional assays |
The Journal of biological chemistry |
High |
29907569
|
| 2023 |
PRMT1 methylates PHGDH at R236, enhancing its catalytic activity to promote serine biosynthesis, which ameliorates oxidative stress and supports HCC tumor growth; a non-methylatable TAT-tagged peptide blocking PHGDH methylation inhibits HCC in PDX models. |
In vitro methylation assay, PHGDH enzymatic activity assay, metabolomics, site-directed mutagenesis, PDX tumor model |
Nature communications |
High |
36823188
|
| 2024 |
FBXO7 E3 ubiquitin ligase binds PRMT1, ubiquitinates it at K37, and promotes its proteasomal degradation, thereby suppressing PRMT1-mediated PHGDH methylation and serine synthesis in HCC. |
Co-IP, ubiquitination assay, site-directed mutagenesis, proteasome inhibitor treatment, in vivo HCC models |
Nature communications |
High |
38839752
|
| 2023 |
PRMT1 methylates cGAS at the conserved R133 residue, preventing cGAS dimerization and suppressing cGAS/STING innate immune signaling in cancer cells; PRMT1 ablation or inhibition restores cGAS/STING signaling, elevates interferon responses, and enhances anti-tumor immunity. |
In vitro methylation assay, cGAS dimerization assay, PRMT1 KO/inhibitor, type I/II IFN reporter assays, in vivo tumor immune infiltration |
Nature communications |
High |
37193698
|
| 2021 |
PRMT1-mediated meR342-EZH2 methylation promotes PRC2 assembly by preventing AMPKα1-mediated pT311-EZH2 phosphorylation, enhancing EZH2-SUZ12 interaction, and repressing P16 and P21 transcription to promote breast cancer cell proliferation. |
In vitro methylation, Co-IP, site-directed mutagenesis, ChIP, cell cycle analysis, xenograft |
Cell death & disease |
High |
34775498
|
| 2021 |
PRMT1 regulates SCYL1 arginine methylation at the γ2-COP-binding site, which is required for SCYL1 interaction with γ2-COP and COPI vesicle formation; PRMT1 co-localizes with SCYL1 in the Golgi fraction, and PRMT1 inhibition disrupts Golgi morphology, axon outgrowth, and dendrite complexity. |
In vitro methylation assay, Co-IP, subcellular fractionation, siRNA rescue with methylation-site mutant, Golgi morphology imaging |
Molecular biology of the cell |
High |
32583741
|
| 2021 |
PRMT1 suppresses MHC-I surface expression by limiting STAT1 expression and activation; PRMT1 knockout or type I PRMT inhibition enhances IFN-γ-induced MHC-I expression, and PRMT1 re-introduction reverses this effect. |
CRISPR-Cas9 screen, PRMT1 KO, pharmacological inhibition (GSK3368715), flow cytometry for MHC-I, STAT1 activity assays |
Cell reports |
High |
38401121
|
| 2022 |
PRMT1 regulates androgen receptor (AR) recruitment to genomic target sites; PRMT1 inhibition impairs AR binding at lineage-specific enhancers, decreasing expression of AR target oncogenes including AR itself in prostate cancer. |
Genome-scale CRISPR-Cas9 screen, ChIP-seq, PRMT1 KO/inhibition, AR target gene expression |
Cell reports |
High |
35196489
|
| 2023 |
CDK5 phosphorylates PRMT1 at S307, promoting PRMT1 translocation from nucleus to cytoplasm and lysosome in response to amino acids; cytoplasmic PRMT1 then methylates WDR24, an essential GATOR2 component, to activate mTORC1 signaling and promote tumor growth. |
Co-IP, kinase assay, subcellular fractionation, in vitro methylation assay, site-directed mutagenesis, xenograft |
Cell reports |
High |
36995937
|
| 2021 |
PRMT1 ablation in vascular smooth muscle cells (VSMCs) causes aortic dissection by downregulating contractile gene expression; PRMT1 directly regulates myocardin gene activation through modulation of H4R3me2a epigenetic histone marks at the myocardin promoter. |
VSMC-specific conditional KO mice, ChIP, ex vivo aortic contractility assay, gene expression profiling |
Experimental & molecular medicine |
High |
34635781
|
| 2020 |
PRMT1 regulates epicardial EMT and invasion by controlling splicing of Mdm4; loss of PRMT1 leads to p53 accumulation that enhances Slug degradation and blocks EMT, establishing a PRMT1-p53 pathway required for epicardial lineage formation. |
Epicardial-specific Prmt1 KO, scRNA-seq, Mdm4 splicing analysis, p53 and Slug protein analysis |
Cell reports |
High |
32521264
|
| 2019 |
PRMT1 is required for maintenance of mature β-cell identity; its deletion causes immediate loss of H4R3me2a and subsequent reduction in chromatin accessibility at binding sites for CTCF and β-cell transcription factors, leading to diabetes. |
β-cell-specific PRMT1 KO, ChIP-seq, ATAC-seq, H4R3me2a histone mark analysis |
Diabetes |
High |
31848151
|
| 2023 |
PRMT1 methylates SRSF1 at arginine residues; this methylation is critical for SRSF1 phosphorylation, RNA binding, and exon inclusion; PRMT1 overexpression promotes aberrant exon inclusion in breast cancer, and PRMT1 inhibition with iPRMT1 blocks this splicing program. |
In vitro methylation assay, PRMT1 methylome profiling, RNA splicing analysis, PRMT1 inhibitor treatment |
Cell reports |
High |
37938975
|
| 2017 |
Kinetic analysis reveals PRMT1 operates by a sequential ordered Bi-Bi mechanism; the perceived degree of processivity depends on both cofactor and enzyme concentration, and substrate sequence influences kinetic parameters. |
Steady-state enzyme kinetics, varied substrate and cofactor concentrations, synthetic peptides |
Chembiochem |
High |
29112789
|
| 2021 |
Cancer-associated mutations W215L, Y220N, and M224V in the PRMT1 dimerization arm disrupt oligomer formation and substantially impair both SAM binding and methyltransferase activity, as shown by AUC, native PAGE, and activity assays. |
Site-directed mutagenesis, analytical ultracentrifugation, native PAGE, in vitro methyltransferase activity assay, molecular dynamics simulations |
The Journal of biological chemistry |
High |
34688662
|
| 2017 |
BTG1 interacts with ATF4 and recruits PRMT1 to methylate ATF4 at R239, positively modulating ATF4 transcriptional activity and stress response; loss of BTG1 impairs this modification and provides a survival advantage under cellular stress. |
Co-IP, in vitro methylation assay, Btg1 knockout MEFs, stress survival assay |
Oncotarget |
Medium |
26657730
|
| 2023 |
PRMT1 methylates WTAP at arginine residues; this promotes WTAP activity as a component of the m6A methyltransferase complex, leading to m6A modification of NDUFS6 mRNA, upregulation of oxidative phosphorylation, and multiple myeloma tumorigenesis. |
Co-IP, in vitro methylation assay, m6A-seq/MeRIP, PRMT1 knockdown, cell proliferation assays |
Cell death & disease |
Medium |
37558663
|
| 2024 |
PRMT1 methylates PHGDH at R54 or R20 in TNBC cells, activating PHGDH enzymatic activity by stabilizing 3-phosphoglycerate binding and suppressing polyubiquitination; concurrently, PRMT1 methylates PFKFB3 and PKM2, diverting glucose toward serine synthesis pathways and increasing palmitate production via FASN to drive chemoresistance. |
In vitro methylation assay, 13C metabolic flux analysis, site-directed mutagenesis, IHC with imaging MS in clinical specimens |
Cancer research |
High |
38383964
|
| 2024 |
PRMT1 induces arginine methylation of DDX3, enhancing its protein stability by preventing proteasomal degradation; DDX3 then translocates to mitochondria and facilitates PINK1 translation to coordinate mitophagy and mitochondrial biogenesis, supporting breast cancer metastasis. |
Co-IP, in vitro methylation assay, proteasome inhibitor treatment, mitochondrial fractionation, PINK1 translation assay |
Cancer research |
High |
39042374
|
| 2024 |
PRMT1 methylates PGK1 at R206, which enhances phosphorylation of PGK1 at S203, inhibiting mitochondrial function and promoting glycolysis in colorectal cancer. |
In vitro methylation assay, site-directed mutagenesis, phosphorylation analysis, metabolic assays |
Cell death & disease |
Medium |
38402202
|
| 2020 |
PRMT1 methylates SMARCA4R1157W mutant more efficiently than WT SMARCA4 due to enhanced SMARCA4 recruitment to H4R3me2a; the R1157W mutation in SMARCA4 facilitates chromatin remodeling by enhancing its ATPase activity within the SWI/SNF complex. |
Co-IP, ChIP, ATPase activity assay, CRISPR mutation introduction, CRC cell and PDX organoid assays |
NPJ precision oncology |
Medium |
36922568
|
| 2023 |
PRMT1 methylates c-Fos at R287; this modification protects c-Fos from autophagic degradation, stabilizing c-Fos protein and enhancing AP-1 transcriptional activity to promote gastric tumorigenesis. |
Co-IP, in vitro methylation assay, site-directed mutagenesis, autophagy inhibition, AP-1 reporter assay |
International journal of biological sciences |
Medium |
37564212
|
| 2022 |
PRMT1 methylates BRD4 at R179/181/183 (antagonized by demethylase JMJD6), and this methylation promotes BRD4 phosphorylation; BRD4 methylation is also associated with TGF-β signaling and ovarian cancer invasion. |
Co-IP, in vitro methylation assay, site-directed mutagenesis, JMJD6 demethylation assay |
Cell death & disease |
Medium |
37737256
|
| 2022 |
PRMT1 directly interacts with and methylates SOX2; EphA2 increases PRMT1 expression and activity, and PRMT1-mediated SOX2 methylation induces cancer stemness and chemoresistance in SCLC. |
Co-IP, GST pulldown, in vitro methylation assay, EphA2 mutant analysis, PDX model |
Cancer science |
Medium |
36377249
|
| 2020 |
PRMT1 methylates progesterone receptor (PR) at R637, reducing PR stability and accelerating its recycling, thereby increasing PR transcriptional activity and expression of progesterone-inducible genes in breast cancer cells. |
Co-IP, in vitro methylation assay, site-directed mutagenesis, PRMT1 depletion, PR target gene analysis |
iScience |
Medium |
32563156
|
| 2024 |
PRMT1 promotes glycolysis (Warburg effect) in NSCLC by upregulating PTBP1, which increases the PKM2/PKM1 ratio; p53 activation under glucose-deficient conditions suppresses USP7 and thereby promotes polyubiquitin-dependent degradation of PRMT1. |
PRMT1 knockdown/overexpression, PTBP1 and PKM splicing analysis, USP7 inhibitor, p53 activation assays |
Cell death & disease |
Medium |
39009589
|
| 2021 |
PRMT1 methylates STAT3 at R688; TIPE1 binds to the catalytic domain of PRMT1 and inhibits this methylation, thereby decreasing STAT3 transactivation and suppressing osteosarcoma malignancy. |
Co-IP, in vitro methylation assay, TIPE1 overexpression, STAT3 reporter assay |
Cell death & disease |
Medium |
36151091
|
| 2025 |
PRMT1 methylates PARP1, which on one hand promotes PARP1-mediated DNA damage repair; on the other hand, it modulates NF-κB signaling via P65 activation to enhance tumor stemness and immune suppression, driving lung metastasis and chemoresistance in TNBC. |
Mass spectrometry, Co-IP, in vitro methylation assay, P65 signaling analysis, functional metastasis assays |
Research (Washington, D.C.) |
Medium |
40927753
|
| 2018 |
RANKL treatment increases PRMT1 expression and nuclear localization in bone marrow-derived macrophages in a JNK-dependent manner; PRMT1 regulates NF-κB transcriptional activity by directly interacting with NF-κB subunit p65, promoting osteoclastogenesis. |
siRNA knockdown, Co-IP (PRMT1-p65), RANKL signaling assays, haploinsufficient mice, in vivo OVX bone loss model |
Experimental & molecular medicine |
Medium |
30154485
|
| 2008 |
TR3 orphan receptor physically interacts with PRMT1 through the catalytic domain and inhibits PRMT1 methyltransferase activity; reciprocally, PRMT1 binding stabilizes TR3 protein and enhances its transcriptional activity independently of methyltransferase activity. |
Co-IP, in vitro methyltransferase activity inhibition assay, TR3 knockdown/KO cells, luciferase reporter |
Nucleic acids research |
Medium |
19095693
|
| 2024 |
LPCAT2 arrests PRMT1 in the cytoplasm of CRC cells by regulating acetylation of PRMT1 at K145, thereby preventing nuclear PRMT1-mediated SLC7A11 transcriptional activation and inducing ferroptosis. |
scRNA-seq, Co-IP, acetylation analysis, PRMT1 localization fractionation, PRMT1 knockout mice CRC model |
Oncogene |
Medium |
38605214
|