Affinage

Showing SACK1D — FAM83D is a alias.

SACK1D

Annotated
2026-06-10
62 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SACK1D/FAM83D is a mitotic spindle adaptor protein that scaffolds kinases and motor machinery onto the spindle to ensure correct chromosome behavior and spindle positioning during cell division (PMID:18485706, PMID:31338967). It localizes to the mitotic spindle, where it recruits the chromokinesin Kid to generate polar ejection forces and organize the metaphase plate; loss of FAM83D or Kid causes chromosomes to collapse onto monopolar spindle poles (PMID:18485706). Through its C-terminal α-helix it targets CK1α to the spindle, and a CK1α-binding-deficient mutant (F283A) produces spindle positioning defects and prolonged mitosis that are rescued by artificially retargeting CK1α to the spindle (PMID:31338967). HMMR binds this same C-terminal helix, is required for assembly of the FAM83D-CK1α complex at the spindle and for correct spindle alignment, and stabilizes FAM83D against ubiquitination; mitotic hyperphosphorylation of FAM83D, also dependent on the C-terminal helix, signals its proteasomal destruction at mitotic exit, consistent with a phosphorylation-exposed C-terminal degron (PMID:41550726). A separate intrinsically disordered region containing four tandem TQT motifs binds the LC8 dynein light chain, with the first TQT dominating recruitment in an "anchored flexibility" mode (PMID:26652654). In cancer contexts FAM83D acts as an oncogenic driver: it physically binds FBXW7 and promotes its ubiquitination and degradation, stabilizing FBXW7 substrates and activating downstream signaling, and FBXW7-binding-site mutations abolish FAM83D-driven proliferation, invasion, and tumor growth (PMID:24344117, PMID:38454442). Targeting CK1α and FAM83D for co-degradation through the CUL4A-CRBN E3 ligase is achievable with lenalidomide-derived molecular glues, dependent on the direct CK1α-FAM83D interaction [PMID:bio_10.1101_2025.06.17.660125].

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 2008 High

    Established FAM83D (CHICA) as a mitotic spindle protein that physically recruits the chromokinesin Kid to drive polar ejection forces and metaphase plate organization, defining its first concrete mitotic function.

    Evidence Reciprocal Co-IP, siRNA depletion, double-depletion epistasis, and monastrol monopolar spindle assay with live-cell imaging

    PMID:18485706

    Open questions at the time
    • Did not identify the spindle-targeting determinant within FAM83D
    • Phosphorylation observed during mitosis but kinases and sites not mapped
  2. 2013 Medium

    Identified the FAM83D-FBXW7 physical interaction as the route by which FAM83D elevates FBXW7 oncogenic substrates (mTOR), linking the spindle protein to oncogenic signaling.

    Evidence Co-IP, overexpression/knockdown, rapamycin rescue, migration/invasion assays

    PMID:24344117

    Open questions at the time
    • FBXW7-binding region on FAM83D not mapped
    • Mechanism of FBXW7 downregulation (degradation vs transcription) not resolved here
  3. 2015 High

    Structurally resolved how an intrinsically disordered FAM83D region engages the LC8 dynein light chain, defining the molecular grammar of its TQT-motif recognition.

    Evidence NMR, ITC, and X-ray crystallography of LC8-peptide complexes

    PMID:26652654

    Open questions at the time
    • Functional consequence of LC8 binding for FAM83D mitotic activity not tested
    • Whether LC8 binding is regulated by mitotic phosphorylation unknown
  4. 2017 Medium

    Connected FAM83D physically to the HMMR/TPX2/AURKA spindle module and showed it is required for microtubule regrowth, reinforcing its role as a microtubule-associated mitotic factor.

    Evidence Co-IP with HMMR, TPX2, AURKA and microtubule regrowth assay after nocodazole washout

    PMID:29088801

    Open questions at the time
    • Direct vs indirect nature of each interaction not distinguished
    • No structural or domain mapping of the HMMR interaction at this stage
  5. 2019 High

    Defined FAM83D as the spindle-targeting adaptor for CK1α via its C-terminal residue F283, establishing a kinase-recruitment mechanism for spindle positioning and timely mitosis.

    Evidence CRISPR knockin of F283A, knockout rescue, artificial CK1α spindle retargeting, live-cell spindle positioning assay

    PMID:31338967

    Open questions at the time
    • Spindle substrates of recruited CK1α not identified
    • Did not address what stabilizes the FAM83D-CK1α complex at the spindle
  6. 2020 Medium

    Generalized FAM83D's CK1α-destabilizing activity to a non-mitotic, differentiation context, implicating a putative PLD-like domain in regulating CK1α and ERK signaling.

    Evidence GFP localization, domain-deletion (PLD-like) analysis, Western blots of differentiation and signaling markers, proteasome inhibition in muscle cells

    PMID:32092437

    Open questions at the time
    • PLD-like domain catalytic activity not biochemically demonstrated
    • Single-lab muscle model, generality unclear
  7. 2024 High

    Mapped the FBXW7-binding sites on FAM83D and showed they are essential for FAM83D-promoted FBXW7 ubiquitination/degradation and for its full oncogenic phenotype, cementing the FBXW7 axis as a core driver function.

    Evidence Systematic mutagenesis, Co-IP, ubiquitination assays, in vitro functional assays, xenograft model

    PMID:38454442

    Open questions at the time
    • How FAM83D promotes FBXW7 ubiquitination mechanistically (recruited E3, autoubiquitination) not defined
    • Relationship between spindle and oncogenic FBXW7 functions of the same protein unresolved
  8. 2025 High

    Identified HMMR as a binding partner of the FAM83D C-terminal α-helix that is required for FAM83D-CK1α complex formation and spindle alignment and that stabilizes FAM83D, while linking mitotic hyperphosphorylation to a C-terminal degron controlling mitotic-exit destruction.

    Evidence Co-IP, C-terminal helix deletion mapping, phosphosite mapping, live-cell spindle alignment and protein stability assays

    PMID:41550726

    Open questions at the time
    • The E3 ligase and degron recognition machinery acting at mitotic exit not identified
    • Which mitotic kinase hyperphosphorylates FAM83D not established
  9. 2025 Medium

    Demonstrated FAM83D and CK1α can be co-degraded by CRBN-based molecular glues in a manner dependent on their direct interaction, validating the FAM83D-CK1α complex as a pharmacological handle.

    Evidence Molecular glue degrader treatment, proteasome inhibitor rescue, CRBN/CUL4A validation, patient-derived cells carrying a CK1α-binding-deficient mutant as control (preprint)

    PMID:bio_10.1101_2025.06.17.660125

    Open questions at the time
    • Preprint, not peer-reviewed
    • Whether co-degradation has therapeutic consequences in cancer not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How FAM83D's mitotic spindle/CK1α-adaptor role mechanistically connects to its oncogenic FBXW7-degrading activity, and what substrates the spindle-recruited CK1α phosphorylates, remain unresolved.
  • No unified model linking spindle adaptor and FBXW7-degradation functions
  • Spindle CK1α substrates unidentified
  • E3 ligase mediating mitotic-exit destruction of FAM83D unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0008092 cytoskeletal protein binding 2 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1640170 Cell Cycle 3 R-HSA-392499 Metabolism of proteins 2
Partners
AURKACSNK1A1DYNLL1FBXW7GSK3BHMMRKIF22TPX2
Complex memberships
FAM83D-CK1α spindle complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 CHICA (FAM83D) localizes to the mitotic spindle, is upregulated and phosphorylated during mitosis, and is required for proper metaphase plate organization and polar ejection forces. CHICA co-immunoprecipitates with the chromokinesin Kid and is required for Kid's spindle localization (but not its chromosome association). Depletion of CHICA or Kid (or both) causes chromosomes to collapse onto poles of monastrol-induced monopolar spindles. Co-immunoprecipitation, siRNA depletion, live-cell imaging, monopolar spindle assay Current biology : CB High 18485706
2015 The LC8 dynein light chain binds to a 69-residue intrinsically disordered region of CHICA (FAM83D) that contains four tandem TQT motifs. Crystal structures show that the first TQT motif dominates LC8 recruitment with rigidly fixed TQT-LC8 contacts, while non-TQT interactions are flexible. This defines an 'anchored flexibility' model for LC8 motif recognition. NMR (secondary chemical shifts, relaxation), isothermal titration calorimetry, X-ray crystallography of LC8–peptide complexes Biochemistry High 26652654
2013 FAM83D physically interacts with FBXW7, downregulates FBXW7 expression, and thereby elevates levels of FBXW7 oncogenic substrates including mTOR. Inhibition of mTOR by rapamycin suppresses FAM83D-induced cell migration and invasion. Co-immunoprecipitation, ectopic overexpression and siRNA knockdown, rapamycin inhibitor treatment, migration/invasion assays Oncotarget Medium 24344117
2019 FAM83D recruits CK1α to the mitotic spindle. Cells lacking FAM83D, or bearing CK1α-binding-deficient FAM83D(F283A) knockin mutations, display pronounced spindle positioning defects and prolonged mitosis. Restoring FAM83D at the endogenous locus or artificially delivering CK1α to the spindle rescues these defects, establishing FAM83D as the spindle-targeting adaptor for CK1α during mitosis. CRISPR/Cas9 knockin (F283A mutation), FAM83D knockout rescue, artificial spindle targeting of CK1α, live-cell imaging, spindle positioning assay EMBO reports High 31338967
2019 FAM83D activates the PI3K/AKT/mTOR pathway in ovarian cancer cells; overexpression promotes proliferation and invasion while inhibiting autophagy, and these effects are suppressed by the mTOR inhibitor Torin1. siRNA knockdown and ectopic overexpression, Western blot (PI3K, AKT, mTOR, P62), Torin1 inhibitor rescue, xenograft mouse model Acta biochimica et biophysica Sinica Medium 30939187
2017 FAM83D knockdown in colorectal cancer cells upregulates FBXW7 protein and reduces Notch1 protein. FBXW7 siRNA reverses suppression of Notch1 by FAM83D knockdown, and Notch1 overexpression reverses the anti-proliferative and anti-migratory effects of FAM83D knockdown, placing FAM83D upstream of the FBXW7/Notch1 axis. siRNA knockdown, epistasis rescue with FBXW7 siRNA and Notch1 overexpression, Western blot, migration/invasion assays Biomedicine & pharmacotherapy Medium 28407575
2015 FAM83D activates the MEK/ERK signaling pathway and promotes S-phase entry in hepatocellular carcinoma cells; forced FAM83D expression enhances proliferation while knockdown has the opposite effect. Ectopic overexpression, siRNA knockdown, Western blot (p-MEK, p-ERK), cell cycle analysis Biochemical and biophysical research communications Medium 25646692
2017 FAM83D co-immunoprecipitates with HMMR, TPX2, and AURKA in gastric cancer cells, and FAM83D knockdown inhibits microtubule regrowth after nocodazole washout, supporting its role as a microtubule-associated protein involved in mitosis. Co-immunoprecipitation, microtubule regrowth assay after nocodazole washout, siRNA knockdown Oncotarget Medium 29088801
2016 FAM83D inhibition in lung adenocarcinoma cells causes G1-phase arrest with downregulation of cyclin D1 (CCND1) and cyclin E1 (CCNE1), indicating that FAM83D promotes G1/S cell-cycle progression. siRNA knockdown, flow cytometry cell cycle analysis, Western blot (cyclin D1, cyclin E1), xenograft model American journal of cancer research Medium 27904773
2020 FAM83D overexpression in NSCLC cells activates the AKT/mTOR pathway to promote EMT, invasion, and cisplatin resistance; pharmacological inhibition of AKT or mTOR reverts FAM83D-induced tumorigenic phenotypes. Retroviral/lentiviral stable overexpression and knockdown, Western blot, AKT/mTOR inhibitor treatment, xenograft model Cellular oncology Medium 32006253
2020 In skeletal muscle cells, Fam83d overexpression represses myosin heavy chain and myogenin expression and suppresses phosphorylated ERK and AKT. The putative PLD-like domain of Fam83d is required for destabilizing CK1α and inhibiting ERK phosphorylation. Fam83d is induced during neurogenic muscle atrophy and localizes in a punctate cytoplasmic pattern in C2C12 cells. GFP-fusion localization, ectopic overexpression, domain-deletion analysis (PLD-like domain), Western blot (p-ERK, p-AKT, myogenin, MyHC), 26S proteasome inhibition Cellular signalling Medium 32092437
2021 Fam83D knockdown in pancreatic cancer cells reduces nuclear β-catenin, c-Myc, and LDHA levels and suppresses aerobic glycolysis; a Wnt/β-catenin inhibitor abolishes the effects of Fam83D overexpression, placing Fam83D upstream of the Wnt/β-catenin pathway. siRNA knockdown and overexpression, Wnt/β-catenin inhibitor rescue, Western blot (β-catenin, c-Myc, LDHA), Seahorse metabolic assay, xenograft model Life sciences Medium 33571515
2022 YTHDF2, an m6A reader, negatively regulates FAM83D protein expression in lung adenocarcinoma. YTHDF2 knockdown promotes migration and invasion through upregulation of FAM83D and consequent activation of the TGFβ1-SMAD2/3 pathway. Proteomic analysis of YTHDF2 KD cells, Western blot, migration and invasion assays, pathway rescue Frontiers in oncology Low 35186724
2023 METTL3 physically interacts with FAM83D and mediates m6A modification of FAM83D mRNA, positively regulating FAM83D protein expression. METTL3 knockdown decreases FAM83D expression and inhibits Wnt/β-catenin pathway activation in triple-negative breast cancer. Co-immunoprecipitation (METTL3-FAM83D), m6A modification assay, Western blot, overexpression rescue experiments, xenograft model Toxicology in vitro Medium 38043628
2024 Systematic mutational analysis mapped FBXW7-binding sites on FAM83D. Mutations at these sites abolish FAM83D's ability to promote FBXW7 ubiquitination and proteasomal degradation, and eliminate FAM83D-driven cell proliferation, migration, invasion, and tumor growth, establishing these sites as essential for FAM83D's oncogenic function. Comprehensive mutational analysis, co-immunoprecipitation, ubiquitination assays, in vitro functional assays, xenograft model Breast cancer research : BCR High 38454442
2022 FAM83D silencing in glioblastoma cells decreases phosphorylated AKT and phosphorylated mTOR levels; AKT inhibitor MK2206 abolishes FAM83D overexpression-driven proliferation, and β-catenin re-expression reverses FAM83D-knockdown-induced anti-tumor effects, placing FAM83D upstream of the AKT/Wnt/β-catenin pathway. siRNA knockdown, MK2206 AKT inhibitor rescue, β-catenin re-expression rescue, Western blot, xenograft model Environmental toxicology Medium 35150198
2022 FAM83D promotes hepatocellular carcinoma cell proliferation and migration by inhibiting FBXW7-mediated degradation of MCL1. FBXW7 siRNA or MCL1 overexpression reverse the effects of FAM83D knockdown on proliferation and apoptosis, and FBXW7 expression is inversely correlated with both FAM83D and MCL1 in patient data. siRNA knockdown and overexpression, epistasis with FBXW7 siRNA and MCL1 overexpression, Western blot, apoptosis assay Translational cancer research Medium 36388033
2025 HMMR binds to the C-terminal α-helix of SACK1D/FAM83D, co-localizes with the SACK1D-CK1α complex throughout mitosis, and is required for SACK1D-CK1α complex formation at the spindle and for correct spindle alignment. HMMR binding stabilizes SACK1D. Mitotic hyperphosphorylation of SACK1D signals its destruction upon mitotic exit, a process that also requires the C-terminal α-helix, suggesting hyperphosphorylation exposes a C-terminal degron. Co-immunoprecipitation, domain mapping (C-terminal helix deletion), phosphosite mapping, live-cell imaging, spindle alignment assay, protein stability assay iScience High 41550726
2025 HMMR interacts with FAM83D (via co-immunoprecipitation and mass spectrometry) and stabilizes FAM83D by inhibiting its ubiquitination. This HMMR-FAM83D interaction modulates β-catenin levels, driving NPC progression through Wnt/β-catenin signaling. Co-immunoprecipitation, mass spectrometry, Western blot, ubiquitination assay, RNA-seq, xenograft model Scientific reports Medium 41083782
2025 FoxM1 directly transcriptionally activates FAM83D in cervical adenocarcinoma (validated by ChIP-seq, qPCR, and luciferase reporter assay). FoxM1 governs cell cycle progression and proliferation via FAM83D-dependent pathways. Additionally, FoxM1 physically interacts with KPNA2 (co-immunoprecipitation). ChIP-seq, luciferase reporter assay, qPCR, co-immunoprecipitation Life sciences Medium 40345484
2025 FAM83D directly interacts with GSK3β (co-immunoprecipitation), promotes GSK3β Ser9 phosphorylation (inactivation), and thereby stabilizes Snail to drive EMT and metastasis in cervical cancer. AKT and PKA are upstream kinases in FAM83D-mediated GSK3β inactivation. GSK3β inhibition reverses the anti-metastatic effects of FAM83D knockdown. Co-immunoprecipitation, Western blot (pSer9-GSK3β, Snail), siRNA knockdown, GSK3β inhibitor rescue, in vivo lung/liver metastasis model Biology direct Medium 41882663
2025 In the context of targeted protein degradation, lenalidomide-derived molecular glue degraders DEG-77 and SJ3149 co-degrade SACK1D/FAM83D along with CK1α via the CUL4A-CRBN E3 ligase complex and the proteasome. This co-degradation requires direct CK1α-SACK1D interaction, as the CK1α-binding-deficient SACK1D/FAM83D is not co-degraded in cells from palmoplantar keratoderma patients. Molecular glue degrader treatment, proteasome inhibitor rescue, CRBN/CUL4A validation, patient-derived cell lines with R265P SACK1G mutation as negative control bioRxivpreprint Medium bio_10.1101_2025.06.17.660125
2026 Knockdown of FAM83D in glioma causes abnormal cell division leading to accumulation of cytoplasmic double-stranded DNA, which activates the cGAS-STING signaling pathway to induce tumor cell senescence. FAM83D-depleted cells also produce a SASP that promotes senescence in neighboring cells and drives macrophage polarization toward an M1 state via ANXA1-FPR1/2 ligand-receptor signaling. siRNA knockdown, cGAS-STING pathway Western blot/reporter, single-cell transcriptome sequencing, cell co-culture model, in situ allograft mouse model, cytoplasmic dsDNA detection Journal of experimental & clinical cancer research Medium 41742219

Source papers

Stage 0 corpus · 62 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2015 Chitosan-tripolyphosphate nanoparticles as Arrabidaea chica standardized extract carrier: synthesis, characterization, biocompatibility, and antiulcerogenic activity. International journal of nanomedicine 69 26089666
2013 FAM83D promotes cell proliferation and motility by downregulating tumor suppressor gene FBXW7. Oncotarget 68 24344117
2017 miRNA-495 suppresses proliferation and migration of colorectal cancer cells by targeting FAM83D. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 54 29221726
2015 FAM83D activates the MEK/ERK signaling pathway and promotes cell proliferation in hepatocellular carcinoma. Biochemical and biophysical research communications 48 25646692
2008 The spindle protein CHICA mediates localization of the chromokinesin Kid to the mitotic spindle. Current biology : CB 47 18485706
2017 FAM83D knockdown regulates proliferation, migration and invasion of colorectal cancer through inhibiting FBXW7/Notch-1 signalling pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 45 28407575
2020 circFOXM1 promotes proliferation of non-small cell lung carcinoma cells by acting as a ceRNA to upregulate FAM83D. Journal of experimental & clinical cancer research : CR 41 32228656
2015 Upregulation of FAM83D affects the proliferation and invasion of hepatocellular carcinoma. Oncotarget 40 26125229
2019 FAM83D directs protein kinase CK1α to the mitotic spindle for proper spindle positioning. EMBO reports 37 31338967
2020 FAM83D promotes epithelial-mesenchymal transition, invasion and cisplatin resistance through regulating the AKT/mTOR pathway in non-small-cell lung cancer. Cellular oncology (Dordrecht, Netherlands) 33 32006253
2021 Fam83D promotes tumorigenesis and gemcitabine resistance of pancreatic adenocarcinoma through the Wnt/β-catenin pathway. Life sciences 32 33571515
2019 FAM83D inhibits autophagy and promotes proliferation and invasion of ovarian cancer cells via PI3K/AKT/mTOR pathway. Acta biochimica et biophysica Sinica 31 30939187
1997 A new phospholipase A2 isoform isolated from Bothrops neuwiedii (Yarará chica) venom with novel kinetic and chromatographic properties. Toxicon : official journal of the International Society on Toxinology 30 9278970
2015 The Anchored Flexibility Model in LC8 Motif Recognition: Insights from the Chica Complex. Biochemistry 29 26652654
2018 The extended production of UV-induced reactive oxygen species in L929 fibroblasts is attenuated by posttreatment with Arrabidaea chica through scavenging mechanisms. Journal of photochemistry and photobiology. B, Biology 27 29156345
2015 Evaluation of anti-inflammatory, antiangiogenic and antiproliferative activities of Arrabidaea chica crude extracts. Journal of ethnopharmacology 26 25683298
2016 Upregulation of FAM83D promotes malignant phenotypes of lung adenocarcinoma by regulating cell cycle. American journal of cancer research 25 27904773
2017 FAM83D, a microtubule-associated protein, promotes tumor growth and progression of human gastric cancer. Oncotarget 24 29088801
2019 Effects of Extract of Arrabidaea chica Verlot on an Experimental Model of Osteoarthritis. International journal of molecular sciences 22 31547612
1999 Characterization of a basic phospholipase A2-homologeu myotoxin isolated from the venom of the snake Bothrops neuwiedii (yarará chica) from Argentina. Toxicon : official journal of the International Society on Toxinology 22 10519651
2022 YTHDF2 Inhibits the Migration and Invasion of Lung Adenocarcinoma by Negatively Regulating the FAM83D-TGFβ1-SMAD2/3 Pathway. Frontiers in oncology 18 35186724
2020 Identification of NUF2 and FAM83D as potential biomarkers in triple-negative breast cancer. PeerJ 18 33005492
2019 FAM83D promotes ovarian cancer progression and its potential application in diagnosis of invasive ovarian cancer. Journal of cellular and molecular medicine 17 31037837
2016 FAM83D associates with high tumor recurrence after liver transplantation involving expansion of CD44+ carcinoma stem cells. Oncotarget 17 27769048
2012 Meta-analysis of the expression of the mitosis-related gene Fam83D. Oncology letters 17 23205133
2013 Evaluation of the mutagenicity and genotoxicity of Arrabidaea chica Verlot (Bignoneaceae), an Amazon plant with medicinal properties. Journal of toxicology and environmental health. Part A 15 23557236
2015 Evaluation of Safety of Arrabidaea chica Verlot (Bignoniaceae), a Plant with Healing Properties. Journal of toxicology and environmental health. Part A 14 26383782
2021 Carajurin: a anthocyanidin from Arrabidaea chica as a potential biological marker of antileishmanial activity. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 12 34323692
2012 Cloning and functional expression of secreted phospholipases A(2) from Bothrops diporus (Yarará Chica). Biochemical and biophysical research communications 12 22995294
2022 Inhibition of FAM83D displays antitumor effects in glioblastoma via down-regulation of the AKT/Wnt/β-catenin pathway. Environmental toxicology 11 35150198
2022 Therapeutic Potential of Leaves from Fridericia chica (Bonpl.) L. G. Lohmann: Botanical Aspects, Phytochemical and Biological, Anti-Inflammatory, Antioxidant and Healing Action. Biomolecules 11 36139047
2021 Immune implication of FAM83D gene in hepatocellular carcinoma. Bioengineered 11 34308751
2020 Knockdown of FAM83D Enhances Radiosensitivity in Coordination with Irradiation by Inhibiting EMT via the Akt/GSK-3β/Snail Signaling Pathway in Human Esophageal Cancer Cells. OncoTargets and therapy 11 32547096
2020 Electrospun PCL-based nanofibers Arrabidaea chica Verlot - Pterodon pubescens Benth loaded: synergic effect in fibroblast formation. Biomedical materials (Bristol, England) 11 32955022
2021 The aqueous extract of Fridericia chica grown in northern Colombia ameliorates toxicity induced by Tergitol on Caenorhabditis elegans. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 10 33626396
2020 Standardized Arrabidaea chica Extract Shows Cytoprotective Effects in Zoledronic Acid-Treated Fibroblasts and Osteoblasts. Clinical, cosmetic and investigational dentistry 10 32848479
2019 Effect of Arrabidaea chica extract against chemically induced breast cancer in animal model. Acta cirurgica brasileira 10 31826147
2022 Suppression of FAM83D Inhibits Glioma Proliferation, Invasion and Migration by Regulating the AKT/mTOR Signaling Pathway. Translational oncology 9 35617811
2021 Protective Effects of the Hydroethanolic Extract of Fridericia chica on Undifferentiated Human Neuroblastoma Cells Exposed to α-Zearalenol (α-ZEL) and β-Zearalenol (β-ZEL). Toxins 9 34822532
2022 miRNA-142-3p functions as a potential tumor suppressor directly targeting FAM83D in the development of ovarian cancer. Aging 8 35489022
2022 FAM83D promotes the proliferation and migration of hepatocellular carcinoma cells by inhibiting the FBXW7/MCL1 pathway. Translational cancer research 8 36388033
2020 Fam83d modulates MAP kinase and AKT signaling and is induced during neurogenic skeletal muscle atrophy. Cellular signalling 8 32092437
2023 Systematic analysis of the oncogenic role of FAM83D across cancers based on data mining. Cell cycle (Georgetown, Tex.) 7 36710419
2023 METTL3 regulates FAM83D m6A modification to accelerate tumorigenesis of triple-negative breast cancer via the Wnt/β-catenin pathway. Toxicology in vitro : an international journal published in association with BIBRA 7 38043628
2021 Arrabidaea chica Verlot fractions reduce MIA-induced osteoarthritis progression in rat knees. Inflammopharmacology 7 33881683
2022 High-Resolution Mass Spectrometry Identification and Characterization of Flavonoids from Fridericia chica Leaves Extract with Anti-Arbovirus Activity. Molecules (Basel, Switzerland) 6 36144777
2024 The FBXW7-binding sites on FAM83D are potential targets for cancer therapy. Breast cancer research : BCR 4 38454442
2023 Cytoprotective, Antiproliferative, and Anti-Oxidant Potential of the Hydroethanolic Extract of Fridericia chica Leaves on Human Cancer Cell Lines Exposed to α- and β-Zearalenol. Toxins 4 36668856
2024 FAM83D acts as an oncogene by regulating cell cycle progression via multiple pathways in synovial sarcoma: a potential novel downstream target oncogene of anlotinib. Discover oncology 3 38512482
2022 Arrabidaea chica chloroform extract modulates estrogen and androgen receptors on luminal breast cancer cells. BMC complementary medicine and therapies 3 35057779
2022 Cytoprotective effect of Fridericia chica (Bonpl.) L.G. Lohmann extract associated with geranylgeraniol enriched-fraction from Bixa orellana L. on epithelial cells treated with bisphosphonate. Natural product research 3 36226767
2021 The role of spray-drying atmosphere on fridericia chica (bonpl.) L.G. Lohmann standardized extract production for wound healing activity. Natural product research 2 34875942
2025 FoxM1 promotes the proliferation of cervical adenocarcinoma cells through transcriptional activation of FAM83D. Life sciences 1 40345484
2024 Immunomodulatory and Anticancer Effects of Fridericia chica Extract-Loaded Nanocapsules in Myeloid Leukemia. Pharmaceutics 1 38931948
2022 Anti-Mayaro virus activity of a hydroethanolic extract from Fridericia chica (Bonpl.) L. G. Lohmann leaves. Journal of ethnopharmacology 1 36067840
2026 Targeting FAM83D triggers tumor cell senescence via cGAS-STING signaling activation and reprograms TAMs to combat glioma. Journal of experimental & clinical cancer research : CR 0 41742219
2026 FAM83D facilitates EMT and metastasis of cervical cancer via interaction with GSK3β and inactivation of GSK3β/stabilization of Snail signaling. Biology direct 0 41882663
2025 HMMR mediates progression of nasopharyngeal carcinoma by inhibiting FAM83D ubiquitination and activating beta-catenin signaling pathway. Scientific reports 0 41083782
2025 Healing Oral Mucositis With Arrabidaea chica Verlot Mucoadhesive Gel in Patients Undergoing Hematopoietic Stem Cell Transplantation: A Randomized Controlled Clinical Trial. BioMed research international 0 41394293
2025 HMMR/RHAMM recruits SACK1D/FAM83D-CK1α complex at the mitotic spindle to control spindle alignment. iScience 0 41550726
2024 FAM83D promotes the progression of 4NQO-induced esophageal carcinoma via inhibiting FBWX7. Experimental cell research 0 39260674
2021 Dynamic expression of FAM83D in peripheral organs at different ages in mice. Gene expression patterns : GEP 0 34325035

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