Affinage

PLAAT4

Phospholipase A and acyltransferase 4 · UniProt Q9UL19

Length
164 aa
Mass
18.2 kDa
Annotated
2026-06-10
35 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PLAAT4 (TIG3/RARRES3) is a Ca2+-independent phospholipase A1/A2 and acyl protein thioesterase that functions as a tumor suppressor and effector of keratinocyte terminal differentiation (PMID:19615464, PMID:24867881). Its catalytic activity resides in the N-terminal hydrophilic domain (residues ~1–134), which is sufficient for phospholipase A2 activity and adopts an H-REV107-like fold, while the C-terminal hydrophobic domain dictates subcellular localization rather than catalysis (PMID:20100577, PMID:25871522, PMID:11078805). The protein partitions between two functional sites: at membranes its C-terminal domain drives plasma membrane targeting where it binds and activates type I transglutaminase to promote cornified envelope formation (PMID:11078805, PMID:17762858, PMID:18612777), whereas an N-terminal motif directs it to the centrosome, where it co-localizes with γ-tubulin and pericentrin, suppresses centrosome separation, alters microtubule dynamics, and restrains proliferation while triggering apoptotic markers (PMID:24401997, PMID:21858038, PMID:22427689). As an acyl protein thioesterase, RARRES3 deacylates Wnt proteins and LRP6 to suppress Wnt/β-catenin signaling, EMT, and cancer stem cell properties downstream of p53, and its enzymatic activity limits breast cancer lung metastasis (PMID:25361079, PMID:24867881). Its expression is induced by retinoids through RAR-dependent transcription and is repressed by MEK-ERK signaling, by the histone modifiers G9a (H3K9me2) and KDM2A (H3K36me2 demethylation), and by the transcription factor BCL6 (PMID:12879006, PMID:15856468, PMID:28532996, PMID:35697678, PMID:40777995). Additional effector interactions include RPLP0 (mediating cell cycle arrest and apoptosis) and MTDH (suppressing metastasis), and RARRES3 functions as an IFNγ-stimulated gene that restricts Toxoplasma gondii by inducing premature parasite egress (PMID:31131438, PMID:26269758, PMID:34871166).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2000 High

    Established that the C-terminal hydrophobic domain is required for membrane/perinuclear localization and for the protein's growth-suppressive activity, the first link between localization and function.

    Evidence GFP-fusion localization and colony formation assays of full-length vs. C-terminal truncation mutants in CHO, T47D and HaCaT cells

    PMID:11078805

    Open questions at the time
    • Did not define the catalytic basis of growth suppression
    • Did not identify molecular partners
  2. 2003 Medium

    Defined the upstream transcriptional control, showing TIG3 induction by retinoic acid is RAR-dependent and accompanies suppression of transformed growth.

    Evidence RAR antagonist treatment and RT-PCR with anchorage-independent colony assays in HNSCC and NSCLC cells

    PMID:12879006

    Open questions at the time
    • Direct RAR binding to the promoter not demonstrated
    • Did not connect transcription to a downstream enzymatic mechanism
  3. 2005 Medium

    Identified MEK-ERK signaling as a negative regulator of TIG3 expression, with an additional IFNγ-reversible MEK-independent route in some cells.

    Evidence MEK inhibition, IFNγ treatment, RT-PCR and in situ hybridization in ovarian carcinoma cells

    PMID:15856468

    Open questions at the time
    • Did not identify the transcription factor coupling MEK-ERK to the locus
    • MEK-independent mechanism left undefined
  4. 2008 Medium

    Provided a molecular effector mechanism for differentiation by showing TIG3 binds and activates type I transglutaminase to drive cornified envelope formation.

    Evidence Co-immunoprecipitation, transglutaminase activity assay and epidermal immunofluorescence (with reciprocal co-precipitation and truncation mapping in companion work)

    PMID:17762858 PMID:18612777

    Open questions at the time
    • Did not establish whether phospholipase activity is required for TG1 activation
    • Structural basis of the 112–164 interaction interface unresolved
  5. 2009 High

    Defined the core biochemical activity, showing recombinant TIG3 is a Ca2+-independent phospholipase with PLA1 predominating over PLA2 and minor acyltransferase activity.

    Evidence In vitro enzymatic assays with purified recombinant protein and substrate specificity profiling

    PMID:19615464

    Open questions at the time
    • Physiological substrate(s) in cells not identified
    • Did not link enzymatic output to specific cellular phenotypes
  6. 2010 High

    Localized catalysis to the N-terminal hydrophilic domain, separating enzymatic function from the localization role of the C-terminus.

    Evidence Truncated N-terminal domain expression, in vitro phospholipase assay and limited proteolysis mapping

    PMID:20100577

    Open questions at the time
    • Catalytic residues not pinpointed in this study
    • No structure available at this stage
  7. 2012 Medium

    Resolved the centrosomal mechanism, showing pericentrosomal TIG3 colocalizes with γ-tubulin/pericentrin, alters microtubule nucleation and tubulin modifications, and blocks centrosome separation to limit proliferation.

    Evidence Immunofluorescence co-localization, microtubule dynamics and tubulin-modification assays, centrosome separation counting and proliferation assays (building on 2011 SCC-13 findings)

    PMID:21858038 PMID:22427689

    Open questions at the time
    • Direct centrosomal binding partner not identified
    • Whether phospholipase activity drives the microtubule effects unresolved
  8. 2013 Medium

    Established dual localization signals, mapping an N-terminal (1–135) centrosome-targeting segment distinct from the C-terminal membrane/mitochondrial signal.

    Evidence GFP-fusion isolated-domain constructs, fluorescence microscopy and subcellular fractionation in keratinocytes

    PMID:24401997

    Open questions at the time
    • The trans-acting factors that read each targeting signal are unknown
    • Switch between membrane and centrosome pools not characterized
  9. 2014 High

    Demonstrated that phospholipase activity itself is anti-metastatic and uncovered a distinct thioesterase activity that deacylates Wnt/LRP6 to suppress Wnt signaling and EMT downstream of p53.

    Evidence Active-site mutant rescue with in vivo metastasis models; co-IP of RARRES3 with Wnt/LRP6, active-site mutagenesis, acylation and EMT/stemness assays, p53 modulation

    PMID:24867881 PMID:25361079

    Open questions at the time
    • Direct demonstration of thioester bond cleavage on endogenous Wnt in vivo limited
    • Relationship between PLA and thioesterase active sites unresolved
  10. 2015 Medium

    Solved the NMR structure of the N-terminal domain and identified MTDH and (later) RPLP0 as effector partners, while showing the NTD-CTD modulatory logic differs from the H-REV107 paralog.

    Evidence NMR solution structure with domain cell-death assays; co-IP and in vivo metastasis assays for MTDH; Y2H/co-IP/co-localization with functional phenocopy for RPLP0

    PMID:25871522 PMID:26269758 PMID:31131438

    Open questions at the time
    • No full-length protein structure
    • Mechanistic basis of RPLP0 and MTDH downregulation not defined
  11. 2017 High

    Identified epigenetic silencing of RARRES3 by G9a-mediated H3K9me2 as a route to cancer progression, and an immune-regulatory role as an endogenous inhibitor of immunoproteasome expression under IRF1/RORA control.

    Evidence ChIP for H3K9me2 at the locus with genetic/pharmacological G9a inactivation and in vivo HCC models; siRNA knockdown with immunoproteasome subunit readouts and IRF1/RORA analysis

    PMID:28051153 PMID:28532996

    Open questions at the time
    • Mechanism linking RARRES3 to immunoproteasome levels not defined
    • Direct vs. indirect transcriptional effects of G9a not fully separated
  12. 2021 Medium

    Extended RARRES3 function to cell-autonomous immunity, showing this IFNγ-stimulated gene restricts Toxoplasma gondii by inducing premature parasite egress.

    Evidence Overexpression screen of 414 ISGs with T. gondii infection and egress assays across multiple human cell lines

    PMID:34871166

    Open questions at the time
    • Molecular mechanism triggering egress unknown
    • Role of phospholipase vs. thioesterase activity in restriction not tested
  13. 2022 High

    Added a second epigenetic repressor, placing RARRES3 downstream of KDM2A-mediated H3K36me2 demethylation in bladder cancer malignancy.

    Evidence ChIP for H3K36me2, KDM2A knockdown, RARRES3 knockdown epistasis, xenografts and KDM2A inhibitor + ATRA combination

    PMID:35697678

    Open questions at the time
    • How H3K36me2 demethylation represses transcription mechanistically not detailed
    • Interplay with G9a/H3K9me2 regulation untested
  14. 2025 Medium

    Broadened post-translational and transcriptional regulation and the partner landscape, identifying CRABP2 as a destabilizer, BCL6 as a transcriptional repressor coupling loss to PI3K/AKT activation, and a TIG3-derived peptide binding the KRAS G12V Switch II.

    Evidence Co-IP and protein stability assays with rescue for CRABP2; CUT&Tag/RNA-seq with knockdown/overexpression and AKT readouts for BCL6; X-ray crystallography of a TIG3 peptide–KRAS G12V complex with viability assays

    PMID:40657374 PMID:40752582 PMID:40777995

    Open questions at the time
    • KRAS interaction is peptide-based, not full-length protein
    • Whether CRABP2-driven degradation and BCL6 repression act in the same tumors unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the phospholipase and thioesterase activities are partitioned between the membrane and centrosomal pools, and which activity drives each phenotype (differentiation, proliferation control, Wnt suppression, pathogen restriction), remains unresolved.
  • No full-length structure linking catalytic sites to localization signals
  • Endogenous lipid and protein substrates in each compartment unidentified
  • Causal requirement of specific catalytic activity for centrosomal and anti-parasitic functions untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016787 hydrolase activity 4 GO:0140098 catalytic activity, acting on RNA 2 GO:0008289 lipid binding 1 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005815 microtubule organizing center 4 GO:0005886 plasma membrane 3 GO:0005829 cytosol 1
Pathway
R-HSA-1640170 Cell Cycle 3 R-HSA-1643685 Disease 3 R-HSA-1266738 Developmental Biology 2 R-HSA-162582 Signal Transduction 2 R-HSA-168256 Immune System 2
Partners
CRABP2KRASLRP6MTDHRPLP0TGM1

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 Purified recombinant TIG3 (PLAAT4) functions as a Ca2+-independent phospholipase A1/2 with maximal activity of 0.53 µmol/min/mg, active on phosphatidylcholines and phosphatidylethanolamines, with PLA1 activity predominating over PLA2. TIG3 also catalyzes N-acylation of PE and O-acylation of lyso-PC at relatively low rates. In vitro enzymatic assay with purified recombinant protein; substrate specificity profiling Biochimica et biophysica acta High 19615464
2010 The N-terminal hydrophilic region of TIG3 (residues 1–134) is sufficient for Ca2+-independent phospholipase A2 enzymatic activity, while the C-terminal hydrophobic region is important for cellular localization rather than catalysis. Expression and purification of truncated N-terminal domain; in vitro phospholipase activity assay; limited proteolysis mapping structural domain boundaries Protein expression and purification High 20100577
2000 The C-terminal hydrophobic domain of TIG3 is required for perinuclear/membrane localization and for full growth-suppressive activity. Truncated TIG3 lacking this domain (TIG3 1–134) redistributes to the cytoplasm and shows partial loss of colony-suppression activity. Vector-mediated expression of full-length vs. C-terminal truncation mutants; GFP-fusion localization by fluorescence microscopy; colony formation assay in CHO, T47D and HaCaT cells International journal of oncology High 11078805
2007 TIG3 interacts with type I transglutaminase (TG1) through a domain spanning amino acids 112–164. The N-terminal conserved region of TIG3 is required for keratinocyte differentiation; its removal converts TIG3 into a proapoptotic protein characterized by cell rounding, membrane blebbing, cytochrome c release, and caspase-3/PARP cleavage. Loss of the N-terminal region also shifts TIG3 to increased membrane association. Co-precipitation of TG1 with TIG3 truncation mutants; apoptosis assays (cytochrome c release, caspase-3/PARP cleavage, p53/p21 levels); fluorescence localization of mutant series The Journal of investigative dermatology High 17762858
2008 TIG3 interacts with and activates type I transglutaminase (TG1) to promote cornified envelope formation during keratinocyte terminal differentiation. TIG3 expression in the suprabasal epidermis is associated with TG1 activation. Co-immunoprecipitation; transglutaminase activity assay; immunofluorescence localization in epidermis Amino acids Medium 18612777
2011 TIG3 localizes near the centrosome in squamous cell carcinoma cells, and pericentrosomal accumulation of TIG3 alters microtubule and microfilament organization, drives pericentrosomal organelle clustering (a hallmark of apoptosis), reduces cyclin D1/E/A, increases p21, elevates Bax, reduces Bcl-XL, and promotes cleavage of procaspase-3/-9 and PARP. Fluorescence microscopy of GFP-TIG3; organelle distribution assays; Western blot for cell-cycle and apoptosis markers in SCC-13 cells expressing TIG3 PloS one Medium 21858038
2012 TIG3 colocalizes with γ-tubulin and pericentrin at the centrosome, alters microtubule nucleation and anterograde growth, increases α-tubulin acetylation and detyrosination, increases insoluble tubulin, drives formation of a peripheral microtubule ring, suppresses centrosome separation (but not duplication), and reduces cell proliferation. Immunofluorescence co-localization with centrosome markers; microtubule dynamics assays; tubulin modification Western blots; centrosome separation counting; proliferation assays Journal of cell science Medium 22427689
2013 The C-terminal hydrophobic domain of TIG3 targets intact TIG3 to the plasma membrane but, when isolated independently, localizes to mitochondria. A segment within the N-terminal hydrophilic region (amino acids 1–135) is necessary and sufficient for centrosomal targeting, indicating dual localization signals for membrane vs. centrosome functions. GFP-fusion constructs of isolated domains; fluorescence microscopy in keratinocytes; subcellular fractionation The Journal of investigative dermatology Medium 24401997
2014 TIG3 distributes to the cell membrane (where it activates TG1 for terminal differentiation) and to the centrosome (where it inhibits centrosome separation during mitosis and alters microtubule function), establishing two spatially distinct mechanisms for controlling keratinocyte proliferation and survival. Immunofluorescence localization; TG1 activity assay; centrosome separation assay; cell proliferation assay (review/synthesis of prior experimental work) The Journal of investigative dermatology Medium 24599174
2014 RARRES3 phospholipase A1/A2 enzymatic activity contributes to tumor cell differentiation; loss of this activity promotes lung metastasis of breast cancer cells. RARRES3 downregulation also facilitates adhesion of tumor cells to the lung parenchyma. Loss-of-function (shRNA knockdown) and re-expression of wild-type vs. catalytically inactive RARRES3 mutants; in vitro adhesion assays; in vivo lung metastasis mouse models EMBO molecular medicine High 24867881
2014 RARRES3 acts as an acyl protein thioesterase that binds Wnt proteins and LRP6, modulates their acylation status, and thereby suppresses Wnt/β-catenin signaling, epithelial-mesenchymal transition, and cancer stem cell properties. Mutation of conserved active-site residues abolishes this deacylation activity. p53 induces RARRES3 expression, linking p53 to Wnt pathway regulation through protein deacylation. Co-immunoprecipitation of RARRES3 with Wnt proteins and LRP6; active-site mutagenesis; acylation status assays; EMT and cancer stem cell phenotype assays; p53 modulation experiments in breast cancer cells Cell death and differentiation High 25361079
2015 RARRES3 interacts with MTDH (metadherin/AEG-1) as determined by co-immunoprecipitation, and their interaction is inversely correlated; RARRES3 suppresses EMT and metastasis of colorectal cancer cells in vitro and in vivo through this suppression of MTDH. Co-immunoprecipitation; knockdown and re-expression in CRC cell lines; transwell/wound healing migration assays; tail-vein xenograft metastasis model American journal of cancer research Medium 26269758
2015 The NMR solution structure of the TIG3 N-terminal domain (NTD) is similar in overall fold to H-REV107 NTD, but the CTD-binding regions on the NTD differ between TIG3 and H-REV107. The TIG3 NTD enhances cell death induced by the CTD, while the H-REV107 NTD is inhibitory; the flexible main loop of H-REV107, but not TIG3, is critical for this NTD-CTD modulatory function. NMR solution structure determination; cell death assays with domain constructs; domain-interaction studies in HeLa cells FEBS letters High 25871522
2016 Overexpression of TIG3 in HCC Hep3B cells suppresses tumor growth in vitro and in vivo via inhibition of ERK1/2 signaling, promoting apoptosis and inhibiting proliferation and migration. TIG3 cDNA overexpression; Western blot for pERK1/2; apoptosis assays; nude mouse xenograft model Tumour biology Low 26951515
2017 G9a histone methyltransferase epigenetically silences RARRES3 through H3K9 di-methylation at the RARRES3 locus, and this silencing is a key downstream mechanism by which G9a promotes HCC progression. Inactivation of G9a (RNAi, CRISPR, or pharmacological) restores RARRES3 expression and suppresses HCC cell proliferation and metastasis. ChIP assay (H3K9me2 at RARRES3 promoter); RNA-seq; G9a shRNA/CRISPR KO; pharmacological inhibition; in vivo nude mouse model Journal of hepatology High 28532996
2017 RARRES3 knockdown increases transcript and protein levels of immunoproteasome subunits (but not constitutive proteasome subunits) in mammary epithelial and breast cancer cell lines, identifying RARRES3 as an endogenous inhibitor of immunoproteasome expression. RARRES3 expression is regulated by IRF1 and is sensitive to RORA depletion. RARRES3 siRNA knockdown; Western blot and RT-qPCR for immunoproteasome subunits; RORA depletion; IRF1 functional analysis Scientific reports Medium 28051153
2019 PLAAT4 physically interacts with the ribosomal protein RPLP0, as identified by yeast two-hybrid screening and confirmed by co-immunoprecipitation and co-localization. PLAAT4 expression suppresses RPLP0 protein levels; cells expressing PLAAT4 or with RPLP0 silenced show similar patterns of decreased cell viability/proliferation, increased cell death, and reduced levels of cell-cycle-associated and anti-apoptotic proteins, indicating that RPLP0 downregulation mediates PLAAT4-induced cell cycle arrest and apoptosis. Yeast two-hybrid screening; co-immunoprecipitation; co-localization by fluorescence microscopy; RPLP0 siRNA knockdown; cell viability/death assays; Western blot for cell-cycle and apoptosis proteins Cell biochemistry and biophysics Medium 31131438
2021 RARRES3 restricts Toxoplasma gondii infection in human cells by inducing premature egress of the parasite. RARRES3 is an IFNγ-stimulated gene whose individual expression is sufficient to restrict parasite growth across multiple human cell lines. Overexpression screen of 414 IFNγ-induced ISGs; T. gondii infection assays; parasite egress assays in multiple human cell lines eLife Medium 34871166
2022 KDM2A (H3K36me2 demethylase) suppresses RARRES3 expression via demethylation of H3K36me2 at the RARRES3 promoter. RARRES3 knockdown attenuates the inhibitory effects of KDM2A depletion on bladder cancer cell malignant phenotypes, placing RARRES3 downstream of KDM2A in an epigenetic regulatory axis. ChIP for H3K36me2 at RARRES3 promoter; KDM2A knockdown; RARRES3 knockdown rescue epistasis; xenograft mouse model; KDM2A inhibitor + ATRA combination treatment Cell death & disease High 35697678
2025 CRABP2 physically binds PLAAT4 and decreases its protein stability; inhibition of PLAAT4 reverses the suppression of NSCLC cell malignant phenotypes and lipid droplet formation caused by CRABP2 knockdown, defining a CRABP2/PLAAT4-mediated lipid metabolic axis in lung cancer progression. Co-immunoprecipitation of CRABP2 and PLAAT4; protein stability assay; PLAAT4 knockdown rescue experiment; lipid droplet quantification; xenograft mouse model Journal of Cancer Medium 40657374
2025 A peptide derived from TIG3 binds near the Switch II domain of KRAS G12V with moderate affinity, induces conformational changes in KRAS G12V as determined by X-ray crystallography, and reduces viability of cancer cell lines harboring KRAS G12V mutation. X-ray crystallography of TIG3 peptide–KRAS G12V complex; binding affinity measurement; cell viability assay Biochimica et biophysica acta. Proteins and proteomics Medium 40752582
2025 BCL6 transcriptionally represses PLAAT4 expression in high-grade serous ovarian cancer (HGSOC), and BCL6-mediated downregulation of PLAAT4 activates the PI3K/AKT signaling pathway to promote tumor cell proliferation, invasion, and migration in vitro and in vivo. CUT&Tag + RNA-seq to identify BCL6 target genes; PLAAT4 knockdown and overexpression; Western blot for PI3K/AKT and EMT markers; xenograft and abdominal metastasis mouse models Frontiers in pharmacology Medium 40777995
2003 TIG3 mRNA induction by ATRA in head and neck and lung carcinoma cells is blocked by pan-RAR antagonist AGN193109 and RARα antagonist Ro 41-5253, demonstrating that TIG3 transcription is regulated through retinoid receptors (RAR-dependent). Induction of TIG3 by ATRA is associated with suppression of anchorage-independent colony formation. Pharmacological RAR antagonist treatment; RT-PCR; anchorage-independent colony formation assay in HNSCC and NSCLC cell lines Oncogene Medium 12879006
2005 TIG3 expression in ovarian carcinoma cells is negatively regulated by an activated MEK-ERK signaling pathway; specific MEK inhibition restores TIG3 mRNA and is correlated with growth inhibition. In a subset of ovarian carcinoma cells, TIG3 suppression is MEK-ERK-independent but can be partially reversed by IFNγ, indicating multiple upstream regulatory mechanisms. MEK-ERK pathway inhibition with small-molecule MEK inhibitors; IFNγ treatment; RT-PCR; cell growth assay; in situ hybridization International journal of cancer Medium 15856468

Source papers

Stage 0 corpus · 35 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 Histone methyltransferase G9a promotes liver cancer development by epigenetic silencing of tumor suppressor gene RARRES3. Journal of hepatology 132 28532996
2009 Characterization of the human tumor suppressors TIG3 and HRASLS2 as phospholipid-metabolizing enzymes. Biochimica et biophysica acta 67 19615464
2014 RARRES3 suppresses breast cancer lung metastasis by regulating adhesion and differentiation. EMBO molecular medicine 62 24867881
2003 Induction of TIG3, a putative class II tumor suppressor gene, by retinoic acid in head and neck and lung carcinoma cells and its association with suppression of the transformed phenotype. Oncogene 43 12879006
2000 The carboxy-terminal hydrophobic domain of TIG3, a class II tumor suppressor protein, is required for appropriate cellular localization and optimal biological activity. International journal of oncology 38 11078805
2007 Localization of the TIG3 transglutaminase interaction domain and demonstration that the amino-terminal region is required for TIG3 function as a keratinocyte differentiation regulator. The Journal of investigative dermatology 30 17762858
2003 RARRES3 expression positively correlated to tumour differentiation in tissues of colorectal adenocarcinoma. British journal of cancer 30 12838316
2001 The class II tumor-suppressor gene RARRES3 is expressed in B cell lymphocytic leukemias and down-regulated with disease progression. Leukemia 29 11587209
2014 TIG3: an important regulator of keratinocyte proliferation and survival. The Journal of investigative dermatology 27 24599174
2015 RARRES3 suppressed metastasis through suppression of MTDH to regulate epithelial-mesenchymal transition in colorectal cancer. American journal of cancer research 26 26269758
2014 Involvement of RARRES3 in the regulation of Wnt proteins acylation and signaling activities in human breast cancer cells. Cell death and differentiation 26 25361079
2019 The Ribosomal Protein RPLP0 Mediates PLAAT4-induced Cell Cycle Arrest and Cell Apoptosis. Cell biochemistry and biophysics 25 31131438
2021 Overexpression screen of interferon-stimulated genes identifies RARRES3 as a restrictor of Toxoplasma gondii infection. eLife 23 34871166
2011 TIG3 tumor suppressor-dependent organelle redistribution and apoptosis in skin cancer cells. PloS one 21 21858038
2022 Histone H3K36me2 demethylase KDM2A promotes bladder cancer progression through epigenetically silencing RARRES3. Cell death & disease 20 35697678
2017 The metastasis suppressor RARRES3 as an endogenous inhibitor of the immunoproteasome expression in breast cancer cells. Scientific reports 20 28051153
2008 TIG3: a regulator of type I transglutaminase activity in epidermis. Amino acids 19 18612777
2005 Decreased expression of type II tumor suppressor gene RARRES3 in tissues of hepatocellular carcinoma and cholangiocarcinoma. World journal of gastroenterology 18 15742394
2010 Expression, purification and biochemical characterization of the N-terminal regions of human TIG3 and HRASLS3 proteins. Protein expression and purification 16 20100577
2015 Structural and functional characterization of tumor suppressors TIG3 and H-REV107. FEBS letters 13 25871522
2005 Suppression of the TIG3 tumor suppressor gene in human ovarian carcinomas is mediated via mitogen-activated kinase-dependent and -independent mechanisms. International journal of cancer 13 15856468
2012 TIG3 interaction at the centrosome alters microtubule distribution and centrosome function. Journal of cell science 10 22427689
2013 Pericentrosomal localization of the TIG3 tumor suppressor requires an N-terminal hydrophilic region motif. The Journal of investigative dermatology 8 24401997
2017 VS-5584 mediates potent anti-myeloma activity via the upregulation of a class II tumor suppressor gene, RARRES3 and the activation of Bim. Oncotarget 7 29254208
2016 The antitumor effect of TIG3 in liver cancer cells is involved in ERK1/2 inhibition. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 7 26951515
2015 RARRES3 regulates signal transduction through post-translational protein modifications. Molecular & cellular oncology 7 27308522
2008 Effects of narrow-band ultraviolet B and tazarotene therapy on keratinocyte proliferation and TIG3 expression. The Journal of dermatology 7 19017044
2012 1H, 13C, and 15N resonance assignments of the N-terminal domain of human TIG3. Biomolecular NMR assignments 6 22290676
2022 Interferon-α2b-Induced RARRES3 Upregulation Inhibits Hypertrophic Scar Fibroblasts' Proliferation and Migration Through Wnt/β-Catenin Pathway Suppression. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 4 36520614
2013 Lewis lung carcinoma progression is facilitated by TIG-3 fibroblast cells. Anticancer research 2 24023311
2026 Transcriptomic landscape of transposable elements reveals LTR7-PLAAT4 as a potential oncogene and therapeutic target in pancreatic adenocarcinoma. Genome research 0 41506784
2025 CRABP2 promotes metastasis and lipid droplet accumulation in non-small cell lung cancer by downregulating PLAAT4. Journal of Cancer 0 40657374
2025 Tazarotene-Induced Gene 3 (TIG3) Induces Apoptosis in Melanoma Cells Through the Modulation of Inhibitors of Apoptosis Proteins. Biomedicines 0 40722819
2025 Structural insights of the complex formed by KRAS G12V and a novel TIG3 peptide. Biochimica et biophysica acta. Proteins and proteomics 0 40752582
2025 BCL6 promotes the progression of high-grade serous ovarian cancer cells by inhibiting PLAAT4. Frontiers in pharmacology 0 40777995

Missed literature

Know a paper Affinage missed for PLAAT4? Flag it for the maintainers and the community.

No submissions yet.