Affinage

FREM1

FRAS1-related extracellular matrix protein 1 · UniProt Q5H8C1

Length
2179 aa
Mass
244.2 kDa
Annotated
2026-06-09
38 papers in source corpus 17 papers cited in narrative 17 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

FREM1 is a multifunctional extracellular matrix protein essential for epidermal–dermal adhesion during embryogenesis, where loss of function produces subepidermal blistering beneath the lamina densa and renal agenesis (PMID:15345741). It localizes to the sublamina densa of basement membranes as part of a reciprocally stabilized ternary complex with FRAS1 and FREM2, in which deposition of all three proteins is mutually dependent—loss of any one coordinately depletes the others—and these proteins assemble into anchoring cords at the dermal–epidermal junction (PMID:16880404, PMID:37047755). FREM1 is secreted from both epithelial and mesenchymal cells, distinguishing it from the exclusively epithelial FRAS1, and can act in epidermal differentiation independently of the Fras1/Grip1 pathway (PMID:15345741, PMID:17240369). Beyond its structural role, FREM1 binds directly to PDGFC and shapes downstream PDGFRα signaling, modulating TIMP1 expression and basement membrane collagen I deposition (PMID:24046351), and it participates genetically in organ morphogenesis pathways shared with GATA4 (lung lobulation) and SLIT3 (renal agenesis) (PMID:23536828). Frem1 expression in cranial neural crest mesenchyme is directly driven by Sonic Hedgehog/GLI signaling, with GLI binding the Frem1 transcriptional start site and FREM1 protein promoting neural crest proliferation (PMID:36495293). A distinct alternatively spliced isoform, TILRR, is a membrane-bound co-receptor for IL-1RI that increases ligand binding, enhances MyD88 recruitment, and potentiates NF-κB activation in a Ras-dependent manner (PMID:19940113), with separable receptor regions controlling MyD88-dependent NF-κB versus Akt-driven cell survival arms (PMID:22262840). FREM1 deficiency causes congenital diaphragmatic hernia in humans and mice through reduced diaphragm cell proliferation (PMID:23221805).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2004 High

    Established FREM1 as an extracellular matrix protein required for epidermal adhesion, and showed it acts independently of the Fras1/Grip1 differentiation pathway since collagen VI and Fras1 deposition remain normal in its absence.

    Evidence ENU mutagenesis mouse genetics with immunostaining and in situ hybridization of head blebs mutants

    PMID:15345741

    Open questions at the time
    • Molecular partners stabilizing FREM1 in the basement membrane not yet defined
    • Mechanism of adhesion function unresolved
  2. 2006 High

    Defined the FRAS1/FREM1/FREM2 ternary complex and its reciprocal codependence, explaining why loss of any single member abolishes all three from the sublamina densa.

    Evidence Targeted Frem1/Frem2/Grip1 gene disruption in mice plus co-expression complex formation assays in transfected cells

    PMID:16880404

    Open questions at the time
    • Stoichiometry and structural architecture of the complex not determined
    • Direct binding interfaces between subunits not mapped
  3. 2006 Medium

    Distinguished FREM1's dual epithelial/mesenchymal secretion and intracellular periderm distribution from FRAS1, supporting a Fras1-independent role in epidermal differentiation.

    Evidence Immunofluorescence and electron microscopy in Fras1-null mouse embryos

    PMID:17240369

    Open questions at the time
    • Functional significance of intracellular FREM1 in periderm unclear
    • No reciprocal validation of independent activity
  4. 2009 High

    Identified the FREM1 isoform TILRR as a membrane-bound IL-1RI co-receptor that amplifies inflammatory signaling, linking the locus to immune regulation beyond its ECM role.

    Evidence Reciprocal co-IP, mutagenesis, NF-κB reporter, ligand-binding, and Ras activation assays

    PMID:19940113

    Open questions at the time
    • Physiological context of TILRR expression not established
    • Relationship between TILRR isoform and ECM FREM1 not reconciled
  5. 2012 High

    Dissected TILRR control of two separable signaling arms—MyD88-dependent NF-κB versus Akt-driven cell survival—through distinct receptor conformational states.

    Evidence Alanine-scanning mutagenesis (R425A, D448A) with caspase-3, Akt, NF-κB, and survival assays

    PMID:22262840

    Open questions at the time
    • Structural basis of conformational switching not solved
    • In vivo relevance of survival vs inflammatory arms untested
  6. 2012 Medium

    Linked FREM1 deficiency to congenital diaphragmatic hernia via reduced diaphragm cell proliferation, expanding its developmental phenotype.

    Evidence ENU-derived eyes2 truncating allele mouse with Frem1 immunostaining and BrdU/Ki67 proliferation assay

    PMID:23221805

    Open questions at the time
    • Molecular driver of the proliferation defect unknown
    • Pathway connecting FREM1 to diaphragm morphogenesis unmapped
  7. 2013 Medium

    Showed FREM1 binds PDGFC and tunes PDGFRα signaling duration and amplitude, providing a signaling-modulatory mechanism linking it to ECM remodeling.

    Evidence Co-IP of FREM1–PDGFC, fibroblast stimulation from Frem1-mutant mice, TIMP1/collagen I quantification

    PMID:24046351

    Open questions at the time
    • Binding interface and affinity not characterized
    • Whether modulation occurs in vivo during morphogenesis unclear
  8. 2013 Medium

    Placed FREM1 in genetic pathways with GATA4 and SLIT3 for lung and kidney morphogenesis through epistasis.

    Evidence Double-mutant mouse crosses with phenotypic scoring of lung lobulation and renal agenesis

    PMID:23536828

    Open questions at the time
    • Biochemical basis of genetic interactions not established
    • Whether interactions are direct or pathway-level unknown
  9. 2015 Low

    Proposed that TILRR calibrates NF-κB signaling by controlling IκBα release from the actin/spectrin cytoskeleton.

    Evidence 3D predictive modelling, in vitro binding/fractionation, and agent-based in silico simulation

    PMID:26110282

    Open questions at the time
    • Largely computational; IκBα–cytoskeleton interaction lacks orthogonal biochemical validation
    • Direct role of TILRR in sequestration not demonstrated
  10. 2017 Medium

    Demonstrated TILRR-IL-1RI co-receptor signaling drives atherosclerotic plaque progression, giving the inflammatory arm a disease phenotype.

    Evidence TILRR knockout mouse and antibody blockade with plaque histomorphometry

    PMID:28920098

    Open questions at the time
    • Cell-type-specific contribution not resolved
    • Mechanistic link from TILRR signaling to monocyte content not fully traced
  11. 2020 Low

    Indicated TILRR overexpression in cervical epithelium drives cytokine secretion that recruits immune cells.

    Evidence TILRR overexpression in HeLa cells with conditioned-medium Transwell and microfluidic migration assays

    PMID:32719797

    Open questions at the time
    • Overexpression with indirect migration readout; no direct binding or epistasis
    • Endogenous TILRR contribution untested
  12. 2022 Medium

    Established that Shh/GLI signaling directly transcribes Frem1 in cranial neural crest, and that FREM1 protein promotes neural crest proliferation, embedding FREM1 in midfacial morphogenesis.

    Evidence In situ hybridization, Gli1 reporter, SHH stimulation, ChIP at Frem1 TSS, and cNCC proliferation assays

    PMID:36495293

    Open questions at the time
    • Downstream effectors of FREM1-induced proliferation unknown
    • Receptor mediating FREM1 proliferative effect unidentified
  13. 2023 Medium

    Identified FREM1 as a direct miR-1825 target whose suppression promotes head and neck squamous cell carcinoma progression, implicating a tumor-suppressive role.

    Evidence Luciferase reporter, microarray, IHC, in vitro phenotype assays, and xenograft

    PMID:37683055

    Open questions at the time
    • Mechanism by which FREM1 restrains tumor phenotypes unknown
    • Whether ECM or signaling function mediates suppression unclear
  14. 2023 Low

    Showed a CSPG6-domain splicing variant predicted to disrupt the β-sheet architecture needed for Fraser complex assembly, connecting genotype to complex integrity.

    Evidence Minigene splicing assay with structural prediction modeling and Sanger validation

    PMID:41923049

    Open questions at the time
    • Structural disruption is computational only
    • No direct complex assembly experiment performed
  15. 2023 Low

    Implicated Frem1 in pulmonary fibrosis via a MyD88/NF-κB/IL-1β positive feedback loop driving macrophage-to-myofibroblast transition.

    Evidence Bleomycin mouse model with Frem1 silencing, qPCR, Western, flow cytometry, and molecular docking

    PMID:41833105

    Open questions at the time
    • Mechanism indirect without biochemical reconstitution
    • Docking is computational; direct Frem1 interactions in the loop unverified
  16. 2025 Medium

    Confirmed FREM1/FRAS1/FREM2 form anchoring cords whose assembly is independent of AMACO (VWA2), refining the boundary of obligate complex partners.

    Evidence AMACO knockout mouse with immunostaining and electron microscopy of anchoring cords

    PMID:37047755

    Open questions at the time
    • Functional role of AMACO association with cords unresolved
    • Other accessory factors at anchoring cords not catalogued

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the structural ECM/Fraser-complex function of FREM1 relates mechanistically to the TILRR isoform's IL-1RI co-receptor activity, and whether they share regulatory or expression control, remains unresolved.
  • No structural model of FREM1 or the Fraser complex
  • Isoform switching control between FREM1 and TILRR unknown
  • Receptor for FREM1's proliferative/signaling effects unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0060089 molecular transducer activity 2 GO:0038024 cargo receptor activity 1
Localization
GO:0031012 extracellular matrix 3 GO:0005576 extracellular region 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-1474244 Extracellular matrix organization 3 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3
Partners
FRAS1FREM2IL1R1MYD88PDGFC
Complex memberships
Fraser complex (FRAS1/FREM1/FREM2)IL-1RI signaling complex (TILRR isoform)

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 FREM1 is an extracellular matrix protein required for epidermal adhesion during embryonic development; loss-of-function mutations cause subepidermal blistering beneath the lamina densa and renal agenesis. Unlike Fras1 and Grip1 mutants, collagen VI and Fras1 deposition in the basement membrane is normal in Frem1 mutants, indicating FREM1 acts independently of Fras1/Grip1 in epidermal differentiation. Mouse genetics (ENU mutagenesis, classic head blebs mutant characterization), immunostaining, in situ hybridization Proceedings of the National Academy of Sciences of the United States of America High 15345741
2006 FREM1 (QBRICK), FRAS1, and FREM2 form a ternary complex localized to the basement membrane sublamina densa; their basement membrane deposition is mutually and reciprocally dependent, such that loss of any one protein (Frem1, Frem2, or Grip1) results in coordinated depletion of all three from the basement membrane. Targeted gene disruption of Frem1/Frem2/Grip1 in mice, immunostaining for basement membrane localization, co-expression and complex formation assay in transfected cells Proceedings of the National Academy of Sciences of the United States of America High 16880404
2006 FREM1 is secreted from both epithelial and mesenchymal cells (unlike FRAS1 which is exclusively epithelial), yet both proteins co-localize in epithelial basement membranes. FREM1 also displays intracellular distribution in periderm cells and basal keratinocytes around E16, and loss of FRAS1 abolishes FREM1 from the basement membrane but not from periderm cells, indicating FREM1 can act independently in epidermal differentiation processes. Immunofluorescence, electron microscopy, analysis of Fras1-null mouse embryos Experimental cell research Medium 17240369
2007 FREM3 basement membrane localization is independent of the FRAS1/FREM1/FREM2 complex; loss of FRAS1 does not deplete FREM3 from the basement membrane, in contrast to FREM1 and FREM2 which are completely abolished, demonstrating that FREM3 is anchored independently despite sharing the same sublamina densa location. Immunostaining of Fras1-null mouse embryos, comparison of Frem1/Frem2/Frem3 localization Matrix biology : journal of the International Society for Matrix Biology Medium 17596926
2009 TILRR (an isoform/alias of FREM1) is a membrane-bound glycosylated protein that acts as a co-receptor for IL-1RI; it is recruited to the IL-1 receptor complex, increases receptor expression and ligand binding, potentiates NF-κB activation, and enhances MyD88 adapter recruitment in a Ras GTPase-dependent manner. Mutagenesis confirmed that TILRR function requires association with the IL-1RI signaling complex. Co-immunoprecipitation, mutagenesis, NF-κB reporter assays, ligand-binding assays, Ras activation assays The Journal of biological chemistry High 19940113
2012 TILRR (FREM1 isoform) promotes IL-1-induced anti-apoptotic signals and reduces caspase-3 activity through the IL-1RI TIR domain. Alanine-scanning mutagenesis identified two functionally separable regions: R425A blocked Akt activation and cell survival but not MyD88-dependent NF-κB; D448A blocked MyD88-dependent NF-κB but not cell survival, demonstrating that TILRR controls distinct downstream signaling arms through different receptor conformational states. Alanine-scanning mutagenesis, caspase-3 activity assay, Akt kinase assay, NF-κB reporter assay, cell survival assays The Journal of biological chemistry High 22262840
2013 FREM1 binds directly to PDGFC, and this interaction regulates downstream PDGFRα signaling. Fibroblasts from Frem1-mutant mice show shorter duration and amplitude of PDGFC-induced signaling, and PDGFC-stimulated Timp1 expression is reduced, leading to decreased basement membrane collagen I deposition. Co-immunoprecipitation (FREM1–PDGFC binding), fibroblast stimulation assays from Frem1-mutant mice, TIMP1/collagen I quantification Disease models & mechanisms Medium 24046351
2013 Genetic epistasis experiments in mice revealed that FREM1 interacts genetically with GATA4 in lung lobulation defect development and with SLIT3 in renal agenesis development, placing FREM1 in pathways shared with these factors for organ morphogenesis. Double-mutant mouse crosses (Frem1 x Gata4; Frem1 x Slit3), phenotypic scoring of lung lobulation and renal agenesis PloS one Medium 23536828
2015 The NF-κB inhibitor IκBα is sequestered to the actin/spectrin cytoskeletal complex in resting cells and is released during IL-1 stimulation through a process controlled by the FREM1 isoform TILRR, providing a mechanism for signal calibration and amplification-sensitive NF-κB regulation. 3D predictive protein modelling, in vitro binding/fractionation assays, agent-based in silico simulation validated against in vitro data PloS one Low 26110282
2017 Genetic deletion of TILRR (FREM1 isoform 2) or antibody blockade of TILRR reduces atherosclerotic plaque development, with decreased monocyte content and increased collagen and smooth muscle cells in lesions, demonstrating that TILRR-IL-1RI co-receptor signaling drives vascular inflammatory disease progression. Genetic knockout mouse model, antibody blocking experiments, plaque histomorphometry JACC. Basic to translational science Medium 28920098
2012 FREM1 deficiency causes congenital diaphragmatic hernia (CDH) in humans and mice; the Frem1(eyes2) mouse (homozygous truncating mutation) develops retrosternal diaphragmatic hernias, and Frem1 is expressed in the anterior developing diaphragm with decreased cell proliferation in Frem1(eyes2) embryos compared to wild-type. Mouse genetics (ENU-derived eyes2 allele), immunostaining for Frem1 expression, cell proliferation assay (BrdU/Ki67) in diaphragm Human molecular genetics Medium 23221805
2022 Frem1 expression in cranial neural crest cell (cNCC) mesenchyme during midfacial morphogenesis is transcriptionally regulated by Sonic Hedgehog (Shh) signaling; GLI transcription factors bind the Frem1 transcriptional start site, SHH ligand stimulation or pathway activation induces Frem1 expression in cNCCs, and FREM1 protein is sufficient to induce cNCC proliferation in a concentration-dependent manner. In situ hybridization, Gli1 reporter assays, SHH ligand stimulation of cNCCs, ChIP (GLI binding at Frem1 TSS), cNCC proliferation assays Developmental dynamics : an official publication of the American Association of Anatomists Medium 36495293
2023 FREM1 is a direct transcriptional target of miR-1825 in head and neck squamous cell carcinoma; luciferase reporter assay confirmed direct miR-1825 binding to FREM1, and miR-1825 overexpression reduced FREM1 expression and promoted cancer cell proliferation, migration, invasion, and tumor formation. MicroRNA target luciferase reporter assay, microarray, FREM1 immunohistochemistry, in vitro cancer phenotype assays, in vivo xenograft Journal of cellular biochemistry Medium 37683055
2020 TILRR (FREM1 isoform) overexpression in cervical epithelial cells causes secretion of pro-inflammatory cytokines/chemokines that promote migration of THP-1 monocytes and MOLT-4 T lymphocytes, as measured by Transwell assay and microfluidic device. TILRR overexpression in HeLa cells, conditioned medium Transwell migration assay, microfluidic device-based migration quantification Frontiers in cell and developmental biology Low 32719797
2023 A splicing variant in FREM1 (c.3274+4A>G) causes exon 18 skipping resulting in a 62 amino acid deletion in the CSPG6 domain; structural modeling predicts this disrupts the stable β-sheet architecture required for FRAS1/FREM multiprotein complex assembly. Minigene splicing assay (in vitro and in silico), structural prediction modeling, Sanger sequencing validation BMC medical genomics Low 41923049
2023 In a bleomycin-induced pulmonary fibrosis model, Frem1 upregulation activates the MyD88/NF-κB signaling pathway and establishes a positive feedback loop amplifying IL-1β production that drives macrophage-to-myofibroblast transition (MMT); genetic ablation of Frem1 confirmed its non-redundant role in this process. Bleomycin mouse model of IPF, Frem1 gene silencing (siRNA/shRNA), qPCR, Western blot, immunofluorescence, flow cytometry, molecular docking International immunopharmacology Low 41833105
2025 Fraser complex proteins (FREM1, FREM2, FRAS1) form anchoring cords in the sublamina densa of the dermal-epidermal junction; AMACO (VWA2) associates with these anchoring cords but is dispensable for their formation or function, as AMACO-deficient mice show no disruption of Fraser complex basement membrane deposition or anchoring cord formation. AMACO knockout mouse generation, immunostaining for Fraser complex proteins, electron microscopy of anchoring cords International journal of molecular sciences Medium 37047755

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 The extracellular matrix gene Frem1 is essential for the normal adhesion of the embryonic epidermis. Proceedings of the National Academy of Sciences of the United States of America 113 15345741
2006 Breakdown of the reciprocal stabilization of QBRICK/Frem1, Fras1, and Frem2 at the basement membrane provokes Fraser syndrome-like defects. Proceedings of the National Academy of Sciences of the United States of America 110 16880404
2009 FREM1 mutations cause bifid nose, renal agenesis, and anorectal malformations syndrome. American journal of human genetics 76 19732862
2011 Heterozygous mutations of FREM1 are associated with an increased risk of isolated metopic craniosynostosis in humans and mice. PLoS genetics 67 21931569
2011 Manitoba-oculo-tricho-anal (MOTA) syndrome is caused by mutations in FREM1. Journal of medical genetics 56 21507892
2006 Overlapping and divergent localization of Frem1 and Fras1 and its functional implications during mouse embryonic development. Experimental cell research 40 17240369
2012 Deficiency of FRAS1-related extracellular matrix 1 (FREM1) causes congenital diaphragmatic hernia in humans and mice. Human molecular genetics 38 23221805
2009 TILRR, a novel IL-1RI co-receptor, potentiates MyD88 recruitment to control Ras-dependent amplification of NF-kappaB. The Journal of biological chemistry 32 19940113
2007 Basement membrane localization of Frem3 is independent of the Fras1/Frem1/Frem2 protein complex within the sublamina densa. Matrix biology : journal of the International Society for Matrix Biology 25 17596926
2012 A genetic polymorphism of FREM1 is associated with resistance against HIV infection in the Pumwani sex worker cohort. Journal of virology 24 22915813
2013 Novel FREM1 mutations expand the phenotypic spectrum associated with Manitoba-oculo-tricho-anal (MOTA) syndrome and bifid nose renal agenesis anorectal malformations (BNAR) syndrome. American journal of medical genetics. Part A 21 23401257
2012 Distinct control of MyD88 adapter-dependent and Akt kinase-regulated responses by the interleukin (IL)-1RI co-receptor, TILRR. The Journal of biological chemistry 21 22262840
2007 Frem3, a member of the 12 CSPG repeats-containing extracellular matrix protein family, is a basement membrane protein with tissue distribution patterns distinct from those of Fras1, Frem2, and QBRICK/Frem1. Matrix biology : journal of the International Society for Matrix Biology 21 17462874
2017 The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular Disease. JACC. Basic to translational science 20 28920098
2015 Computational Modelling of NF-κB Activation by IL-1RI and Its Co-Receptor TILRR, Predicts a Role for Cytoskeletal Sequestration of IκBα in Inflammatory Signalling. PloS one 17 26110282
2017 Novel FREM1 mutations in a patient with MOTA syndrome: Clinical findings, mutation update and review of FREM1-related disorders literature. European journal of medical genetics 15 28111185
2013 Regulation of PDGFC signalling and extracellular matrix composition by FREM1 in mice. Disease models & mechanisms 15 24046351
2013 Novel frem1-related mouse phenotypes and evidence of genetic interactions with gata4 and slit3. PloS one 14 23536828
2021 The Potential Role of FREM1 and Its Isoform TILRR in HIV-1 Acquisition through Mediating Inflammation. International journal of molecular sciences 9 34360591
2020 TILRR Promotes Migration of Immune Cells Through Induction of Soluble Inflammatory Mediators. Frontiers in cell and developmental biology 9 32719797
2021 TILRR (Toll-like Interleukin-1 Receptor Regulator), an Important Modulator of Inflammatory Responsive Genes, is Circulating in the Blood. Journal of inflammation research 8 34594127
2014 Development of monoclonal antibodies to interrogate functional domains and isoforms of FREM1 protein. Monoclonal antibodies in immunodiagnosis and immunotherapy 8 24746155
2022 Integrated Bioinformatics Identifies FREM1 as a Diagnostic Gene Signature for Heart Failure. Applied bionics and biomechanics 6 35726312
2012 Evidence for additional FREM1 heterogeneity in Manitoba oculotrichoanal syndrome. Molecular vision 6 22690109
2023 The Fraser Complex Proteins (Frem1, Frem2, and Fras1) Can Form Anchoring Cords in the Absence of AMACO at the Dermal-Epidermal Junction of Mouse Skin. International journal of molecular sciences 5 37047755
2023 Oncogenic miR-1825 promotes head and neck carcinogenesis via targeting FREM1. Journal of cellular biochemistry 4 37683055
2022 High level of plasma TILRR protein is associated with faster HIV seroconversion. EBioMedicine 3 35339895
2023 Two novel mutations within FREM1 gene in patients with bifid nose. BMC pediatrics 2 38097983
2022 TILRR Aggravates Sepsis-Induced Acute Lung Injury by Suppressing the PI3K/Akt Pathway. Evidence-based complementary and alternative medicine : eCAM 2 36065264
2025 Non-Canonical Splice Site Variant in FREM1 Result in Fetal Renal Agenesis. Clinical genetics 1 40605465
2024 De Novo Missense Mutation in FREM1 Identified in a Chinese Patient with Comorbid Congenital Microtia and Pulmonary Hypoplasia. The Journal of craniofacial surgery 1 39819863
2022 Frem1 activity is regulated by Sonic hedgehog signaling in the cranial neural crest mesenchyme during midfacial morphogenesis. Developmental dynamics : an official publication of the American Association of Anatomists 1 36495293
2026 Sinominine alleviates pulmonary fibrosis by suppressing macrophage-to-myofibroblast transition via inhibition of the Frem1/NF-κB/IL-1β axis. International immunopharmacology 0 41833105
2026 A novel homozygous splicing variant in FREM1 expands the phenotypic spectrum of BNAR syndrome: functional validation and successful PGT-M. BMC medical genomics 0 41923049
2023 Retracted: TILRR Aggravates Sepsis-Induced Acute Lung Injury by Suppressing the PI3K/Akt Pathway. Evidence-based complementary and alternative medicine : eCAM 0 37387989
2023 Variants in FREM1 and trisomy 18 identified in a neonatal progeria patient. Molecular biology reports 0 37470964
2023 Retracted: Integrated Bioinformatics Identifies FREM1 as a Diagnostic Gene Signature for Heart Failure. Applied bionics and biomechanics 0 38075139
2022 Toll-like Interleukin -1 Receptor Regulator (TILRR) Protein, a Major Modulator of Inflammation, is Expressed in Normal Human and Macaque Tissues and PBMCs. Journal of inflammation research 0 35592073

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