Affinage

TP53INP2

Tumor protein p53-inducible nuclear protein 2 · UniProt Q8IXH6

Length
220 aa
Mass
24.0 kDa
Annotated
2026-06-10
41 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

TP53INP2 (DOR) is a nutrient-responsive scaffold protein that couples subcellular localization to dual roles in ribosome biogenesis and autophagy (PMID:19056683, PMID:27172002, PMID:41368677). Under basal conditions it is imported into the nucleus and nucleolus via a C-terminal NLS/NoLS, where nuclear proteasomes degrade most of the pool and where it associates with rDNA and is required for assembly of the RNA polymerase I preinitiation complex, thereby promoting rRNA synthesis and ribosome biogenesis (PMID:27172002, PMID:41368677). Upon starvation or stress, disrupted importin-mediated import together with a conserved C-terminal cytoplasmic retention motif drives cytoplasmic accumulation, an event independent of CRM1 export, ubiquitylation, or acetylation and reinforced by FTO-mediated m6A demethylation that enhances its translation (PMID:41368677). In the cytoplasm TP53INP2 functions as a positive regulator of autophagosome biogenesis: it binds Atg8-family proteins through a LIR motif with structural preference for the GABARAP subfamily, an interaction abrogated by acetylation of a conserved Atg8 lysine, and it directly engages ATG7 to form an LC3B–TP53INP2–ATG7 ternary complex that promotes LC3 lipidation and autophagosome formation (PMID:19056683, PMID:30767704, PMID:38726830). Its ubiquitin-interacting motif allows recruitment of ubiquitinated cargo, enabling p62-independent autophagic degradation, a function confirmed in skeletal muscle where TP53INP2 controls muscle mass through autophagy-dependent protein degradation (PMID:24713655, PMID:31155706). As a selective adaptor it also mediates lipophagy by bridging perilipin 1 to LC3 in adipocytes and regulates adipogenesis by promoting autophagy- and ESCRT-dependent sequestration of GSK3β into late endosomes to activate β-catenin/TCF-LEF signaling (PMID:29593329, PMID:40484366). Independently of autophagy, TP53INP2 sensitizes cells to death receptor–induced apoptosis by acting as a scaffold that bridges ubiquitinated caspase-8 to the ligase TRAF6 via dedicated TRAF6-interacting (TIM) and ubiquitin-interacting (UIM) motifs, promoting caspase-8 polyubiquitination and activation (PMID:30979779).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2008 High

    Established TP53INP2 as a required factor for autophagy that physically links the Atg8 conjugation machinery to autophagosome membranes, defining its core cellular role.

    Evidence Yeast two-hybrid, reciprocal Co-IP, BRET, siRNA knockdown with autophagosome quantification, and microscopy in mammalian cells

    PMID:19056683

    Open questions at the time
    • Did not resolve which LIR residues mediate Atg8 binding
    • Mechanism of nucleus-to-autophagosome relocalization unknown
    • VMP1-dependence not structurally defined
  2. 2012 High

    Mapped the functional architecture, identifying a region containing an NES and a LIR motif and a second conserved region, both required for nuclear exit, transcriptional activity, and autophagy, linking localization control to dual function.

    Evidence Phylogenetic reconstruction plus structure/function mutagenesis with transcription, nuclear export, and autophagy readouts

    PMID:22470510

    Open questions at the time
    • Transcriptional targets not defined at this stage
    • Structural basis of LIR-Atg8 selectivity not addressed
    • Did not distinguish import vs export contributions
  3. 2014 High

    Demonstrated in vivo that TP53INP2 controls skeletal muscle mass specifically through autophagy-dependent, p62-independent degradation of ubiquitinated proteins, establishing physiological relevance.

    Evidence Muscle-specific transgenic overexpression and knockout mice, diabetes and denervation models, autophagy flux assays

    PMID:24713655

    Open questions at the time
    • Cargo-recognition mechanism for ubiquitinated proteins not yet molecularly defined
    • Upstream signals controlling muscle TP53INP2 activity unclear
  4. 2016 High

    Revealed a nuclear/nucleolar function distinct from autophagy: TP53INP2 promotes ribosome biogenesis by associating with rDNA and enabling RNA Pol I preinitiation complex assembly.

    Evidence ChIP at rDNA, nucleolar localization assays, Pol I PIC interaction/assembly assays, rRNA measurements

    PMID:27172002

    Open questions at the time
    • Direct contacts within the Pol I PIC not structurally mapped
    • How nutrient state toggles between nucleolar and autophagic pools not resolved here
  5. 2018 High

    Connected TP53INP2 to adipogenesis through autophagy- and ESCRT-dependent sequestration of GSK3β into late endosomes, linking it to β-catenin/TCF-LEF transcriptional control.

    Evidence Knockout mice, preadipocyte differentiation, late-endosome fractionation, β-catenin/TCF-LEF reporters, ESCRT inhibition

    PMID:29593329

    Open questions at the time
    • Direct GSK3β-TP53INP2 binding interface not defined
    • How ESCRT and autophagy machineries cooperate mechanistically unclear
  6. 2019 High

    Defined an autophagy-independent apoptotic function: TP53INP2 scaffolds TRAF6 and caspase-8 via TIM and UIM motifs to drive caspase-8 polyubiquitination and death receptor sensitivity.

    Evidence Reciprocal Co-IP, TIM/UIM mutagenesis, in vivo mouse liver apoptosis model, TRAIL/FasL assays

    PMID:30979779

    Open questions at the time
    • Ubiquitin chain type on caspase-8 not characterized
    • How apoptotic vs autophagic functions are partitioned not resolved
  7. 2019 High

    Resolved the autophagosome-biogenesis mechanism by showing TP53INP2 directly binds ATG7 to form an LC3B–TP53INP2–ATG7 ternary complex sufficient to trigger LC3 lipidation.

    Evidence Co-IP, GST pulldown, LIR mutant (W35A/I38A), LC3B-PE lipidation assays, colocalization with ATG14/DFCP1/WIPI2

    PMID:30767704

    Open questions at the time
    • Stoichiometry and structure of the ternary complex not determined
    • Whether ATG7 binding is direct at the same surface as LC3 unresolved
  8. 2019 Medium

    Proposed TP53INP2 as a ubiquitin-binding autophagic adaptor via its UIM, capable of competing with p62 for LC3 and routing ubiquitinated cargo.

    Evidence UIM deletion mutagenesis, ubiquitin-binding assays, Co-IP, autophagy flux and chloroquine sensitivity assays

    PMID:31155706

    Open questions at the time
    • Single-lab study without reciprocal in vivo validation
    • Endogenous ubiquitinated substrates not identified
    • Relationship to p62 in physiological contexts unclear
  9. 2024 High

    Defined the localization switch: a C-terminal NLS/NoLS drives import and nucleolar enrichment, while a conserved CRM blocks nuclear re-entry under stress, with starvation disrupting importin-mediated import to enforce cytoplasmic accumulation.

    Evidence CRISPR knockout/EGFP reconstitution, deletion mutagenesis, FRAP, importin-binding assays, proteasome inhibition, ATG5-KO epistasis, m6A/FTO assays

    PMID:41368677

    Open questions at the time
    • The sensor that converts starvation into impaired import not identified
    • How CRM mechanistically blocks re-entry not structurally defined
  10. 2024 High

    Provided the structural and biophysical basis for GABARAP-subfamily selectivity and showed Atg8 acetylation acts as a switch controlling TP53INP2 binding and shuttling.

    Evidence ITC, X-ray crystal structures of TP53INP2-LIR with GABARAP and acetylated/deacetylated LC3A, acetyl-mimetic mutant cell assays

    PMID:38726830

    Open questions at the time
    • The acetyltransferase/deacetylase regulating Atg8 K49 in this context not identified
    • Functional consequence of selectivity for specific cargo not dissected

Open questions

Synthesis pass · forward-looking unresolved questions
  • Multiple tissue- and cancer-context functions (NPM1-mutant AML survival and apoptosis, gastric cancer ZSCAN18 axis, BMSC osteogenesis, DDLPS mitophagy of YAP, adipocyte lipophagy via PLIN1) remain to be integrated into a unified regulatory logic for how TP53INP2's localization and partner choice are selected in each setting.
  • Context-specific upstream regulators largely uncharacterized
  • Mitochondrial localization and VDAC1-dependent mitophagy of YAP rest on a single study
  • Lipophagy adaptor role via PLIN1 not independently confirmed

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0140110 transcription regulator activity 2 GO:0003677 DNA binding 1
Localization
GO:0005634 nucleus 2 GO:0005730 nucleolus 2 GO:0005829 cytosol 2 GO:0005768 endosome 1
Pathway
R-HSA-9612973 Autophagy 3 R-HSA-1266738 Developmental Biology 1 R-HSA-5357801 Programmed Cell Death 1 R-HSA-74160 Gene expression (Transcription) 1
Partners
ATG7CASP8GABARAPGABARAPL2LC3BPLIN1TRAF6VMP1
Complex memberships
LC3B-TP53INP2-ATG7 complex

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 TP53INP2 binds to LC3, GABARAP, and GABARAPL2 (Atg8-family proteins) as well as the autophagosome transmembrane protein VMP1; it translocates from the nucleus to autophagosome structures upon autophagy induction by rapamycin or starvation; siRNA-mediated knockdown strongly decreases autophagosome formation, indicating TP53INP2 is required for autophagy; it is proposed to act as a scaffold recruiting LC3/GABARAP to the autophagosome membrane via VMP1. Yeast two-hybrid screening, co-immunoprecipitation, siRNA knockdown, bioluminescence resonance energy transfer (BRET), fluorescence microscopy Molecular biology of the cell High 19056683
2012 Structure-function analysis identified two conserved regions in DOR/TP53INP2: region 1 (aa 28–42) contains a nuclear export signal (NES) and a functional LC3-interacting region (LIR) motif; mutations in hydrophobic residues of region 1 reduce transcriptional activity and block nuclear exit and autophagic activity. Region 2 (aa 66–112) mutations reduce transcriptional activity, impair nuclear exit upon autophagy activation, and disrupt autophagy. TP53INP1 arose by gene duplication in vertebrates and also regulates autophagy and transcription. Phylogenetic reconstruction, structure/function mutagenesis, nuclear export and transcriptional activity assays PloS one High 22470510
2014 Muscle-specific overexpression of Tp53inp2 in transgenic mice reduces muscle mass, while Tp53inp2 deletion causes muscle hypertrophy. TP53INP2 activates basal autophagy in skeletal muscle and sustains p62-independent autophagic degradation of ubiquitinated proteins. TP53INP2 ablation mitigates experimental diabetes-associated muscle loss, and its overexpression/absence does not affect denervation-induced wasting (where autophagy is blocked), placing TP53INP2 specifically upstream of autophagy-dependent muscle mass regulation. Transgenic mouse models (muscle-specific overexpression and knockout), streptozotocin-induced diabetes model, denervation model, autophagy flux assays The Journal of clinical investigation High 24713655
2016 TP53INP2 localizes to the nucleolus via a C-terminal nucleolar localization signal (NoLS). ChIP assays detect TP53INP2 association with ribosomal DNA (rDNA). Exclusion of TP53INP2 from the nucleolus represses rDNA promoter activity and reduces rRNA and ribosomal protein production. TP53INP2 directly interacts with and is required for assembly of the POLR1/RNA polymerase I preinitiation complex (PIC) at rDNA promoters, revealing a role in promoting ribosome biogenesis. Chromatin immunoprecipitation (ChIP), nucleolar localization assays, RNA polymerase I PIC interaction and assembly assays, rRNA production measurements Autophagy High 27172002
2018 TP53INP2 negatively regulates adipogenesis in preadipocytes by promoting autophagy-dependent sequestration of GSK3β into late endosomes in an ESCRT-dependent manner. This sequestration increases β-catenin levels and enhances TCF/LEF transcriptional activity. TP53INP2 ablation in mice causes enhanced adiposity with greater cellularity of subcutaneous adipose tissue and increased expression of adipogenic master genes. Transgenic mouse models (TP53INP2 knockout), preadipocyte differentiation assays, late endosome fractionation, β-catenin/TCF-LEF reporter assays, ESCRT inhibition experiments Nature cell biology High 29593329
2019 TP53INP2 sensitizes cells to death receptor-induced apoptosis by binding both caspase-8 and the ubiquitin ligase TRAF6, functioning as a scaffold that bridges ubiquitinated caspase-8 to TRAF6 for further polyubiquitination and activation of caspase-8. A TRAF6-interacting motif (TIM) and a ubiquitin-interacting motif (UIM) in TP53INP2 are required; mutations of key TIM residues abrogate TRAF6 and caspase-8 interaction and reduce death receptor-induced apoptosis. TP53INP2 deficiency in cultured cells or mouse livers protects against death receptor-induced apoptosis. Co-immunoprecipitation, site-directed mutagenesis of TIM and UIM motifs, in vivo mouse liver apoptosis model, apoptosis assays with TRAIL/FasL The EMBO journal High 30979779
2019 Cytoplasmic TP53INP2 promotes autophagosome biogenesis by directly interacting with ATG7 to form a LC3B-TP53INP2-ATG7 ternary complex. The N-terminal region of TP53INP2 (including the LIR) is sufficient to trigger LC3B-PE lipidation and autophagosome formation. Loss of TP53INP2-LC3 or TP53INP2-ATG7 interaction significantly reduces LC3B-ATG7 binding. TP53INP2 colocalizes with early autophagic membrane structures (ATG14, DFCP1, WIPI2-positive). Co-immunoprecipitation, GST pulldown, LIR mutant analysis (W35A/I38A), autophagosome formation assays, fluorescence colocalization, LC3B-PE lipidation assays Autophagy High 30767704
2019 TP53INP2 contains a ubiquitin-interacting motif (UIM) that mediates binding to ubiquitin and ubiquitinated proteins. TP53INP2 lacking the UIM can displace the autophagic adaptor p62 from LC3, leading to accumulation of ubiquitinated proteins; overexpression of UIM-deficient TP53INP2 sensitizes cells to chloroquine. This indicates TP53INP2 can act as a novel autophagic adaptor recruiting ubiquitinated substrates to autophagosomes. UIM domain deletion mutagenesis, ubiquitin binding assays, co-immunoprecipitation, autophagy flux assays, chloroquine sensitivity assay FEBS letters Medium 31155706
2009 hnRNP A2 controls alternative splicing of an exon in the 5' UTR of TP53INP2 in a 3D matrix-dependent fashion; this splicing event is required for invasive cell migration into extracellular matrix, with consequences mediated via alterations in Golgi complex integrity during 3D migration. siRNA knockdown of hnRNP A2, exon-tiling microarrays, 3D matrix invasion assays, Golgi morphology analysis Cancer research Medium 19934309
2023 FTO-mediated m6A demethylation upregulates TP53INP2 expression in NPM1-mutated AML cells. Mutant NPM1 directly interacts with TP53INP2 and delocalizes it to the cytoplasm. Cytoplasmic TP53INP2 then enhances autophagy by promoting LC3-ATG7 interaction, facilitating leukemia cell survival. Co-immunoprecipitation (TP53INP2 with mutant NPM1), m6A modification assays (FTO), LC3-ATG7 interaction assays, gain/loss-of-function in AML cells International journal of molecular sciences Medium 36675134
2024 TP53INP2 is predominantly degraded by nuclear proteasomes under basal conditions. Under starvation or chemical stress, TP53INP2 accumulates in the cytoplasm independently of ATG5, CRM1-mediated export, phosphorylation, ubiquitylation, or acetylation. A C-terminal nuclear localization signal (NLS) overlapping a nucleolar localization signal (NoLS) mediates nuclear import and nucleolar enrichment; a conserved nine-amino-acid cytoplasmic retention motif (CRM) in the C-terminus prevents nuclear re-entry under stress. FRAP and importin-binding assays show starvation disrupts nuclear import. Starvation also enhances TP53INP2 translation via FTO-mediated m6A demethylation without altering mRNA stability. CRISPR/Cas9 knockout + EGFP-TP53INP2 reconstitution, deletion mutagenesis, FRAP, importin-binding assays, proteasome inhibitor experiments, ATG5 KO epistasis, m6A/FTO assays Journal of cell science High 41368677
2024 The TP53INP2 LIR motif binds preferentially to GABARAP subfamily proteins over LC3 subfamily proteins. Crystal structures of TP53INP2LIR complexes with GABARAP and LC3A (acetylated and deacetylated) reveal a β-sheet interaction in TP53INP2LIR that determines GABARAP selectivity. Acetylation of the second conserved Lys residue (K49 in LC3B equivalent) in GABARAP or LC3A disrupts interaction with TP53INP2 and impairs nuclear/cytoplasmic LC3 shuttling in cells. Isothermal titration calorimetry (ITC), X-ray crystallography (crystal structures of TP53INP2LIR-GABARAP and TP53INP2LIR-LC3A complexes), acetyl-mimetic mutant cell assays, colocalization studies Autophagy High 38726830
2025 TP53INP2 localizes predominantly to mitochondria in dedifferentiated liposarcoma cells and promotes mitophagic degradation of YAP in a VDAC1-dependent manner. The WW domain of YAP and the PPTY motif of VDAC1 are required for YAP-VDAC1 interaction. TP53INP2 gain/loss-of-function experiments show it inhibits proliferation, migration, stemness, and dedifferentiation of DDLPS cells. Subcellular fractionation/mitochondrial localization, gain/loss-of-function in DDLPS cell lines, domain mutant analysis (WW domain, PPTY motif), mitophagy assays, YAP protein level/activity measurements Oncogene Medium 40185868
2025 In mature adipocytes, TP53INP2 acts as an adaptor protein for lipophagy by directly binding to lipid droplet-associated protein perilipin 1 (PLIN1) and to LC3 via its LIR motif. Co-IP confirmed TP53INP2-PLIN1 interaction. TP53INP2 knockdown impairs lipophagy and prevents PLIN1 degradation, even though general autophagy (p62-LC3) continues, indicating selective lipophagy adaptor function. Co-immunoprecipitation (TP53INP2-PLIN1, TP53INP2-LC3), siRNA knockdown, lipophagy flux assays in 3T3L1 cells, starvation induction Life sciences Medium 40484366
2021 Oxidative stress-induced downregulation of TP53INP2 in BMSCs is mediated by the autophagy-lysosome degradation pathway, as autophagy inhibition with bafilomycin A1 rescues TP53INP2 protein levels. TP53INP2 knockdown inhibits osteogenic differentiation of BMSCs while overexpression promotes it, acting through activation of Wnt/β-catenin signaling (DKK1 abrogated and lithium rescued these effects). siRNA knockdown, overexpression, bafilomycin A1 treatment, Wnt/β-catenin pathway assays, osteogenic differentiation assays in BMSCs and OVX mouse model Free radical biology & medicine Medium 33636337
2023 ZSCAN18 functions as a transcription factor that binds the TP53INP2 promoter and transcriptionally activates TP53INP2 expression in gastric cancer cells. Knockdown of TP53INP2 alleviates the tumor-suppressive effects of ZSCAN18 overexpression, placing TP53INP2 downstream of ZSCAN18 in an autophagy-promoting tumor-suppressive axis. Chromatin immunoprecipitation (ChIP) for ZSCAN18 at TP53INP2 promoter, epistasis by TP53INP2 siRNA knockdown in ZSCAN18-overexpressing cells, in vitro and in vivo tumor assays Clinical epigenetics Medium 36650573
2024 Cytoplasmic TP53INP2 (maintained by mutant NPM1) functions as a scaffold bridging TRAF6 to caspase-8, promoting caspase-8 ubiquitination and activation via the extrinsic apoptosis pathway in AML cells with NPM1 mutations. This was confirmed by co-immunoprecipitation and ubiquitination assays in gain/loss-of-function experiments. Co-immunoprecipitation, ubiquitination assays, gain/loss-of-function experiments, CDX and PDX mouse models, flow cytometry for apoptosis Journal of experimental & clinical cancer research Medium 38909249

Source papers

Stage 0 corpus · 41 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 The TP53INP2 protein is required for autophagy in mammalian cells. Molecular biology of the cell 108 19056683
2014 Autophagy-regulating TP53INP2 mediates muscle wasting and is repressed in diabetes. The Journal of clinical investigation 73 24713655
2009 hnRNP A2 regulates alternative mRNA splicing of TP53INP2 to control invasive cell migration. Cancer research 69 19934309
2021 Oxidative stress induces downregulation of TP53INP2 and suppresses osteogenic differentiation of BMSCs during osteoporosis through the autophagy degradation pathway. Free radical biology & medicine 68 33636337
2019 TP53INP2 contributes to autophagosome formation by promoting LC3-ATG7 interaction. Autophagy 68 30767704
2018 TP53INP2 regulates adiposity by activating β-catenin through autophagy-dependent sequestration of GSK3β. Nature cell biology 57 29593329
2012 DOR/Tp53inp2 and Tp53inp1 constitute a metazoan gene family encoding dual regulators of autophagy and transcription. PloS one 54 22470510
2016 TP53INP2/DOR, a mediator of cell autophagy, promotes rDNA transcription via facilitating the assembly of the POLR1/RNA polymerase I preinitiation complex at rDNA promoters. Autophagy 32 27172002
2019 Regulation of death receptor signaling by the autophagy protein TP53INP2. The EMBO journal 31 30979779
2020 The bifunctional role of TP53INP2 in transcription and autophagy. Autophagy 23 31931658
2023 Cytoplasmic Expression of TP53INP2 Modulated by Demethylase FTO and Mutant NPM1 Promotes Autophagy in Leukemia Cells. International journal of molecular sciences 21 36675134
2020 TP53INP2 Modulates Epithelial-to-Mesenchymal Transition via the GSK-3β/β-Catenin/Snail1 Pathway in Bladder Cancer Cells. OncoTargets and therapy 20 33061441
2024 TP53INP2-dependent activation of muscle autophagy ameliorates sarcopenia and promotes healthy aging. Autophagy 17 38545813
2021 miR-142-3p Regulates Tumor Cell Autophagy and Promotes Colon Cancer Progression by Targeting TP53INP2. Chemotherapy 15 34753133
2017 TP53INP2-related basal autophagy is involved in the growth and malignant progression in human liposarcoma cells. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 15 28131096
2009 TP53INP2 is the new guest at the table of self-eating. Autophagy 15 19145107
2019 TP53INP2 mediates autophagic degradation of ubiquitinated proteins through its ubiquitin-interacting motif. FEBS letters 13 31155706
2023 Inactivation of ZSCAN18 by promoter hypermethylation drives the proliferation via attenuating TP53INP2-mediated autophagy in gastric cancer cells. Clinical epigenetics 12 36650573
2007 The coding region of TP53INP2, a gene expressed in the developing nervous system, is not altered in a family with autosomal recessive non-progressive infantile ataxia on chromosome 20q11-q13. Developmental dynamics : an official publication of the American Association of Anatomists 12 17238154
2022 Overexpression of TP53INP2 Promotes Apoptosis in Clear Cell Renal Cell Cancer via Caspase-8/TRAF6 Signaling Pathway. Journal of immunology research 11 35615533
2020 Dysregulation in the expression of (lncRNA-TSIX, TP53INP2 mRNA, miRNA-1283) in spinal cord injury. Genomics 11 32535070
2019 TP53INP2 Promotes Bovine Adipocytes Differentiation Through Autophagy Activation. Animals : an open access journal from MDPI 11 31810209
2022 TP53INP2 Contributes to TGF-β2-Induced Autophagy during the Epithelial-Mesenchymal Transition in Posterior Capsular Opacification Development. Cells 9 35954230
2015 Is TP53INP2 a critical regulator of muscle mass? Current opinion in clinical nutrition and metabolic care 8 25769060
2024 Autophagic Regulation of Adipogenesis Through TP53INP2: Insights from In Silico and In Vitro Analysis. Molecular biotechnology 6 38238641
2024 Cytoplasmic TP53INP2 acts as an apoptosis partner in TRAIL treatment: the synergistic effect of TRAIL with venetoclax in TP53INP2-positive acute myeloid leukemia. Journal of experimental & clinical cancer research : CR 6 38909249
2019 TP53INP2 at the crossroad of apoptosis and autophagy in death receptor signaling. Molecular & cellular oncology 6 31528702
2012 Extrinsic and intrinsic regulation of DOR/TP53INP2 expression in mice: effects of dietary fat content, tissue type and sex in adipose and muscle tissues. Nutrition & metabolism 6 22995226
2021 Integrative Analysis of TP53INP2 in Head and Neck Squamous Cell Carcinoma. Frontiers in genetics 5 33897760
2023 MicroRNA-362-3p Implicated in Cardioprotection Against Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis by Repressing TP53INP2 and Regulating SDF-1/CXCR4 Pathway. Alternative therapies in health and medicine 4 36933242
2025 The role of TP53INP2 as an adaptor protein in the regulation of lipophagy in mature adipocytes. Life sciences 3 40484366
2024 TP53INP2 knockdown inhibits inflammatory response and apoptosis after spinal cord injury. Immunity, inflammation and disease 3 38652010
2023 TP53INP2 modulates the malignant progression of colorectal cancer by reducing the inactive form of β-catenin. Biochemical and biophysical research communications 3 37995453
2024 RETRACTED: Pachymic acid activates TP53INP2/TRAF6/caspase-8 pathway to promote apoptosis in renal cell carcinoma cells. Environmental toxicology 2 38560766
2024 HIF-3α Facilitates the Proliferation and Migration in Pancreatic Cancer by Inhibiting Autophagy Through Downregulating TP53INP2. Cell biochemistry and biophysics 1 39614944
2026 Salvianolic acid B attenuates cellular senescence and age-related decline in muscle function via dual mTOR/TP53INP2-autophagy regulation. Frontiers in chemistry 0 41867953
2026 Cardiac-derived extracellular vesicles carrying miR-4433b-3p accelerate cognitive decline and brain aging by suppressing TP53INP2-mediated neuronal autophagy in mice. Communications biology 0 42243457
2025 TP53INP2 promotes mitophagic degradation of YAP to impede dedifferentiated liposarcoma development. Oncogene 0 40185868
2025 RETRACTION: Pachymic Acid Activates TP53INP2/TRAF6/Caspase-8 Pathway to Promote Apoptosis in Renal Cell Carcinoma Cells. Environmental toxicology 0 40358478
2025 A C-terminal cytoplasmic retention motif and nuclear localization signal regulates nuclear import of TP53INP2. Journal of cell science 0 41368677
2024 Structural and functional characterization of the role of acetylation on the interactions of the human Atg8-family proteins with the autophagy receptor TP53INP2/DOR. Autophagy 0 38726830

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