Affinage

KLF5

Krueppel-like factor 5 · UniProt Q13887

Length
457 aa
Mass
50.8 kDa
Annotated
2026-06-10
100 papers in source corpus 41 papers cited in narrative 42 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

KLF5 (originally BTEB2/IKLF) is a GC-box-binding zinc-finger transcription factor that programs cell proliferation, differentiation, and lineage fidelity across cardiovascular, epithelial, embryonic, and cancer contexts, acting through three C-terminal zinc fingers that bind Sp1-like GC-rich elements and a proline-rich N-terminal activation domain that contacts the basal transcription machinery (TFIIB, TFIIEβ, TFIIFβ, TBP) (PMID:8479902, PMID:9089417). At target promoters KLF5 directly activates or represses genes spanning vascular and metabolic remodeling—PDGF-A, TGF-β, SMemb/NMHC-B, the lipid-oxidation regulator PPARα, the oxidant source NOX4, and the mitochondrial-protective factor eIF5a—and its loss drives cardiac dysfunction, vascular senescence, and aneurysm phenotypes in tissue-specific knockout mice (PMID:10417400, PMID:12101409, PMID:26574507, PMID:33539225, PMID:32817651). The same factor controls cell-fate decisions: it establishes bipotential ICM/trophectoderm fate in early embryos, maintains intestinal Lgr5+ stem cells and is required for β-catenin-driven oncogenesis, enforces AT2-to-AT1 alveolar differentiation, and governs prostate basal/luminal balance (PMID:34758315, PMID:24626089, PMID:35803279, PMID:32081850). In cancer, KLF5 promotes proliferation, migration, and stemness by activating targets including FYN, COX2, and RAD51 and by nucleating an enhancer machine in which it recruits the CBP/EP300 acetyltransferase complex together with TP63 and YAP1 to deposit H3K27ac, recruit BRD4, and drive Pol II elongation through 3D chromatin loops (PMID:26786295, PMID:36923542, PMID:37702443, PMID:33115806). KLF5 abundance is set by a dense post-translational network: GSK3β-primed phosphodegrons recruit the E3 ligase FBW7 for degradation, WWP1 ubiquitinates the PY motif, and these destabilizing events are opposed by deubiquitinases BAP1 and USP3, by PY-motif competitors YAP, TAZ, and α-Catulin, and by PRMT5-catalyzed arginine methylation that antagonizes GSK3β phosphorylation (PMID:24921010, PMID:26419610, PMID:31624151, PMID:22045023, PMID:22632819, PMID:35154481, PMID:33972717). Acetylation at K369 by the CBP/EP300 axis, reversed by HDAC1/2, additionally toggles KLF5 between proliferative and differentiative outputs and modulates its stability by controlling BAP1 binding (PMID:29679567, PMID:32081850, PMID:35342356). WWP2-mediated monoubiquitination instead activates rather than degrades KLF5 to drive odontoblast differentiation genes, illustrating that distinct ubiquitin marks specify opposite functional fates (PMID:33164644).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 1993 High

    Established the founding biochemical identity of KLF5 as a sequence-specific GC-box transcriptional activator, defining its DNA-binding and transactivation modules.

    Evidence cDNA cloning with recombinant DNA-binding (EMSA), reporter, and GAL4 fusion transactivation assays

    PMID:8479902

    Open questions at the time
    • Physiological target genes not yet identified
    • No cellular or in vivo context
  2. 1997 High

    Localized the activation domain to a short hydrophobic proline/alanine-rich region and showed direct contact with the basal transcription machinery, explaining how KLF5 stimulates transcription.

    Evidence In vitro transcription with purified protein, deletion mutagenesis, pulldown with TFIIB/TFIIEβ/TFIIFβ/TBP

    PMID:9089417

    Open questions at the time
    • Interactions tested in vitro only
    • No coactivator context beyond basal factors
  3. 1999 High

    Connected KLF5 to vascular smooth muscle gene programs and defined its upstream induction by MAPK/Egr-1, placing it within stress-response signaling in the vasculature.

    Evidence EMSA/supershift, GST-DNA binding, reporter mutagenesis on SMemb/SE1 and the Egr-1 site of the KLF5 promoter, MAPK inhibition

    PMID:10417400 PMID:10532946

    Open questions at the time
    • In vivo requirement not yet tested
    • Whether repression vs activation is context-dependent unresolved
  4. 1999 High

    Demonstrated KLF5 can act as a repressor on a CAAT/GT-box target and confirmed nuclear localization, broadening its regulatory repertoire beyond activation.

    Evidence DNase I footprinting, EMSA, GFP localization, reporter assay in endometrial carcinoma cells

    PMID:10572182

    Open questions at the time
    • Determinants of activation vs repression not defined
  5. 2002 High

    Provided the first in vivo genetic evidence that KLF5 drives cardiovascular remodeling through PDGF-A/TGF-β induction and is modulated by RAR, with homozygous loss being embryonic lethal.

    Evidence Heterozygous Klf5 knockout mice, ChIP on PDGF-A, KLF5–RAR co-IP, RAR-ligand pharmacology

    PMID:12101409

    Open questions at the time
    • Cell-type-specific contributions not dissected
    • Mechanism of RAR-dependent modulation incomplete
  6. 2003 High

    Showed CBP coactivation of KLF5 requires PKC-dependent phosphorylation, linking signal-induced phosphorylation to coactivator recruitment.

    Evidence GAL4 transactivation, co-IP, GST pulldown, PKC-site mutagenesis, kinase inhibition

    PMID:12682370

    Open questions at the time
    • Responsible PKC isoform and in vivo phosphosite not defined
    • CBP HAT does not acetylate KLF5 in vitro—acetylating enzyme left open
  7. 2003 High

    Extended KLF5 promoter occupancy to an endogenous immune locus (TCR Dbeta1), confirming functional chromatin binding in a distinct lineage.

    Evidence Yeast one-hybrid, supershift EMSA, ChIP, dominant-negative reporter assay

    PMID:12576331

    Open questions at the time
    • Physiological role in T-cell development not tested in vivo
  8. 2004 Medium

    Revealed that oncogenic Ras switches KLF5 from a cyclin D1-inducing growth promoter to a growth suppressor and destabilizes the protein, introducing the theme of context-dependent KLF5 function.

    Evidence Isogenic Ras-transformed intestinal epithelial cells, colony formation, cyclin D1 reporter, protein stability analysis

    PMID:14726538

    Open questions at the time
    • Molecular basis of the functional switch undefined
    • Single cell-line system
  9. 2014 Medium

    Defined the core degradation machinery for KLF5: GSK3β-phosphorylated CPD degrons recruit FBW7 for ubiquitination, establishing the central phospho-degradation axis.

    Evidence Ubiquitination assay, co-IP, CPD mutagenesis, GSK3β involvement (review integrating primary data)

    PMID:24921010

    Open questions at the time
    • Synthesized from prior primary work
    • Kinase priming hierarchy not fully resolved
  10. 2014 High

    Placed KLF5 within intestinal stem cell maintenance and made it genetically required for β-catenin-driven tumorigenesis, and separately implicated it (with Fli1) in systemic sclerosis pathogenesis.

    Evidence Inducible Lgr5-Klf5 KO with oncogenic β-catenin epistasis; Klf5/Fli1 double-heterozygous mouse fibrosis model

    PMID:24626089 PMID:25504335

    Open questions at the time
    • Direct transcriptional targets in each setting not enumerated
    • Relationship between stem-cell and disease roles unclear
  11. 2012 High

    Identified Hippo effectors YAP and TAZ as KLF5 stabilizers that competitively block WWP1 at the PY motif, coupling Hippo signaling to KLF5 protein levels and target gene output.

    Evidence Co-IP, ubiquitination assays, WW-domain mutants, siRNA, xenografts

    PMID:22045023 PMID:22632819

    Open questions at the time
    • Relative contributions of YAP vs TAZ across tissues not resolved
    • Stoichiometry of competition with WWP1 undefined
  12. 2015 High

    Showed KLF5 directly drives cardiac PPARα and identified BAP1 as a stabilizing deubiquitinase, linking KLF5 to fatty-acid oxidation metabolism and to enzymatic ubiquitin removal.

    Evidence Cardiomyocyte-specific KO with metabolic phenotyping and ChIP; genome-wide DUB screen, DUB assay, in vivo rescue

    PMID:26419610 PMID:26574507

    Open questions at the time
    • c-Jun competition mechanism at the PPARα promoter incompletely mapped
    • BAP1/HCF-1 complex stoichiometry undefined
  13. 2017 High

    Established KLF5 as a transcriptional driver of macrophage podosome formation and migration through Myo9b/RhoA, broadening its role into immune-cell motility and aneurysm pathology.

    Evidence Myeloid-specific KO, Myo9b reporter, migration imaging, RhoA-GTP pulldown

    PMID:28115390

    Open questions at the time
    • Direct vs indirect RhoA regulation not fully separated
  14. 2018 Medium

    Defined acetylation/deacetylation at K369 as a stability and function switch: HDAC1/2-mediated deacetylation promotes degradation while acetyl-mimic blocks it, and showed KLF5 suppresses ERK via Spred1 in ESCs.

    Evidence HDAC1/2 siRNA, K369Q/K369R mutagenesis, CHX chase, MG132, co-IP; Klf5-KO ESCs with paralog-specific rescue and Spred1 analysis; FYN transactivation in bladder cancer

    PMID:26786295 PMID:29679567 PMID:30452437

    Open questions at the time
    • Enzyme depositing K369 acetylation not identified here
    • Single-lab stability data
  15. 2019 High

    Added USP3 as a second stabilizing deubiquitinase, reinforcing that KLF5 levels are set by opposing ligase/DUB activities.

    Evidence Genome-wide DUB screen, co-IP, DUB assay, knockdown-rescue, in vivo tumorigenesis

    PMID:31624151

    Open questions at the time
    • Substrate-site specificity of USP3 vs BAP1 undefined
  16. 2020 High

    Multiple in vivo studies cemented KLF5 as a tissue lineage and metabolic determinant—alveolar AT1 fidelity, prostate basal progenitor maintenance via K369 acetylation, skeletal-muscle atrophy, and FOXO1→KLF5→NOX4 oxidative injury—and revealed a KLF5→eIF5a→Mfn1 axis preserving mitochondrial integrity.

    Evidence Cell-type-specific KO and acetylation knock-in mice, organoids, ChIP, ATAC-seq, AAV rescue, metabolic/ROS readouts

    PMID:32081850 PMID:32817651 PMID:33539225 PMID:34426497 PMID:35803279

    Open questions at the time
    • Upstream selectivity directing KLF5 to opposing differentiation outcomes unclear
    • How a single factor coordinates such divergent tissue programs unresolved
  17. 2020 High

    Resolved how KLF5 amplifies transcription mechanistically: it recruits the CBP/EP300 complex with TP63 and YAP1 to deposit H3K27ac, recruit BRD4, and aggregate distal binding events into 3D loops driving Pol II elongation.

    Evidence IP-MS interactome, HiChIP, H3K27ac/BRD4 ChIP-seq, PROTAC BRD4 degradation, dependency screen

    PMID:33115806

    Open questions at the time
    • Whether this enhancer-machine mode operates outside cancer chromatin untested
  18. 2021 Medium

    Defined arginine methylation as a stabilizing PTM—PRMT5 dimethylates KLF5 (R57 in breast cancer, R41 in lung) to antagonize GSK3β phosphorylation and FBW7 degradation—and clarified acetylation–ubiquitination crosstalk via reduced BAP1 binding.

    Evidence In vitro methylation assays, R57/R41 mutagenesis, PRMT5 inhibitors, PTM crosstalk and BAP1-binding analysis, xenografts

    PMID:33972717 PMID:35342356 PMID:37461162

    Open questions at the time
    • Discrepant methylated residue (R57 vs R41) across tissues not reconciled
    • Some crosstalk data from single labs
  19. 2021 Medium

    Detailed KLF5's combinatorial roles with other factors: opposing AR on chromatin to set basal/luminal prostate programs, partnering YB-1 in basal-like breast cancer, repressing COX2/PGE2 to shape anti-tumor immunity, and dual ICM/TE fate induction in embryos.

    Evidence Chromatin co-IP, ChIP-seq, RNA-seq, mRNA-stability assays, ChIP-seq embryo targets, KO/chimera epistasis, immune profiling

    PMID:34737261 PMID:34758315 PMID:35022570 PMID:36923542

    Open questions at the time
    • Mechanism of KLF5-AR antagonism on shared loci incomplete
    • COX2 axis tested in limited tumor models
  20. 2022 Medium

    Showed ubiquitin-mark identity determines outcome: WWP2 monoubiquitination of KLF5 transactivates rather than degrades it to drive odontoblast differentiation, and α-Catulin competes with WWP1 to stabilize KLF5 in lung cancer stemness.

    Evidence Ubiquitination assays with WWP2 C838A and KLF5 lysine/PY2 mutants, differentiation assays; yeast two-hybrid, co-IP, CHX chase, ILK inhibition

    PMID:33164644 PMID:35154481

    Open questions at the time
    • How mono- vs poly-ubiquitin marks are selected at shared lysines unclear
    • Single-lab data for each interaction
  21. 2023 Medium

    Expanded KLF5's cancer transcriptional partnerships—SRC-phospho-YAP1/TEAD complexes driving Hippo-independent stemness, and an EHF/ELF3-KLF5 complex activating RAD51 to bolster homologous recombination repair.

    Evidence Co-IP, SRC inhibition, phospho-YAP1 mutants, ChIP, super-enhancer analysis, HRR functional assay

    PMID:36633714 PMID:37702443

    Open questions at the time
    • Direct vs indirect assembly of these complexes not fully resolved
    • Single-lab findings
  22. 2024 Medium

    Linked KLF5 to non-cell-autonomous tumor signaling and chromatin metabolism: deacetylated KLF5 downstream of PTEN loss drives a TNF-α/CAF/FGF9/FGFR1 paracrine loop, while lactate-driven H3K14 lactylation promotes KLF5 expression to repress E-cadherin and drive EMT in diabetic kidney disease.

    Evidence Acetylation knock-in mouse with co-culture and pharmacology; ChIP-seq H3K14la, ChIP on cdh1, nephron-specific knockdown

    PMID:38781024 PMID:38925041

    Open questions at the time
    • Generalizability of the paracrine loop beyond PTEN-null prostate cancer untested
    • Lactylation→KLF5 chromatin mechanism single-study

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how a single GC-box factor is directed toward opposite outcomes—proliferation vs differentiation, activation vs repression—across tissues, and how the combinatorial PTM code (phosphorylation, ubiquitination type, acetylation, methylation) is integrated at the level of partner choice and target selection.
  • No unified model linking PTM state to partner/target selection
  • Structural basis of PY-motif competition among YAP/TAZ/α-Catulin/WWP1 undefined
  • Reconciliation of opposing tissue functions absent

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0003677 DNA binding 4 GO:0140223 general transcription initiation factor activity 1
Localization
GO:0005634 nucleus 1 GO:0005654 nucleoplasm 1
Pathway
R-HSA-74160 Gene expression (Transcription) 5 R-HSA-392499 Metabolism of proteins 4 R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3
Partners
ARBAP1EP300FBXW7PRMT5TAZWWP1YAP1
Complex memberships
BAP1/HCF-1 complexKLF5-CBP/EP300 acetyltransferase complexKLF5-EHF-ELF3 complexYAP1/TEAD-KLF5 transcriptional complex

Evidence

Reading pass · 42 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 KLF5 (BTEB2) encodes a GC box-binding protein with three C-terminal zinc finger motifs that binds DNA with specificity similar to Sp1 and activates transcription through a proline/serine/threonine/alanine-rich N-terminal region; recombinant BTEB2 expressed in E. coli showed sequence-specific DNA-binding activity, and cotransfection experiments demonstrated transcriptional activation of GC box-containing reporters. cDNA cloning, recombinant protein DNA-binding assay, cotransfection reporter assay, GAL4 fusion transactivation assay Nucleic acids research High 8479902
1997 The transcriptional activation domain of KLF5 (BTEB2) resides in a ~10-amino-acid hydrophobic, proline/alanine-rich region within the proline-rich N-terminal domain; purified BTEB2 enhanced transcription in an in vitro transcription assay in a GC-box-dependent manner, and this activity was abolished by deletion of the hydrophobic region. Basic transcription factors TFIIB, TFIIEβ, TFIIFβ, and TBP were found to interact with BTEB2 by in vitro binding experiments. In vitro transcription assay with purified protein, deletion/point-mutation analysis, in vitro binding (pulldown) with basal transcription factors Journal of biochemistry High 9089417
1999 KLF5 (BTEB2) binds the SE1 cis-regulatory element in the SMemb/NMHC-B gene promoter and activates its transcription in smooth muscle cells; a GST-BTEB2 fusion protein bound SE1 in a sequence-specific manner, BTEB2 was identified as a major component of the nuclear factor:SE1 complex by gel-shift and antibody supershift, and disruption of SE1 abolished basal and BTEB2-induced promoter activity. Gel mobility shift assay, antibody supershift, GST pulldown/DNA-binding assay, luciferase reporter with site-directed mutagenesis, immunohistochemistry Circulation research High 10417400
1999 KLF5 (BTEB2) expression in vascular smooth muscle cells is transcriptionally activated by PMA and bFGF via an Egr-1 binding site (5'-CGCCCGCGC-3') located at -25 in the BTEB2 promoter, acting through the MAP kinase pathway; site-specific mutation of the Egr-1 site abolished inducible promoter activity. Luciferase reporter assay, site-directed mutagenesis, EMSA (DNA-protein complex characterization), pharmacological inhibition of MAPK pathway Circulation research High 10532946
1999 Full-length human KLF5 (IKLF) encodes a 457-amino-acid nuclear protein that binds the CAAT/GT box (EGFRE) of the mouse lactoferrin gene promoter and represses reporter gene activity in RL95-2 endometrial carcinoma cells; nuclear localization was confirmed by GFP-tagged IKLF transfection and Western fractionation. DNase I footprinting, EMSA, GFP-tagging/fluorescence microscopy, Western blot of nuclear fractions, luciferase reporter assay Nucleic acids research High 10572182
2001 KLF5 (mBTEB2) is a transcriptional target of Wnt-1 signaling; its induction in C57MG cells occurs through a β-catenin/Lef-TCF-independent, PKC-sensitive noncanonical Wnt pathway, as shown by cDNA subtractive hybridization and pharmacological PKC manipulation. cDNA subtractive hybridization, transgenic mouse mammary gland analysis, PKC pharmacological inhibition, reporter assay Molecular and cellular biology Medium 11134343
2002 KLF5 is induced by angiotensin II and in turn activates PDGF-A and TGF-β expression; KLF5 physically interacts with the retinoic acid receptor (RAR), and synthetic RAR ligands modulate KLF5 transcriptional activity; heterozygous Klf5-knockout mice showed diminished cardiovascular remodeling responses, and homozygous knockout caused early embryonic lethality. Heterozygous knockout mouse model, chromatin immunoprecipitation (ChIP) for PDGF-A promoter binding, co-immunoprecipitation (KLF5–RAR interaction), luciferase reporter assay, in vivo pharmacology with RAR ligands Nature medicine High 12101409
2003 KLF5 transactivation is enhanced by CBP; the interaction maps to the N-terminal region of CBP (aa 1–232) and the N-terminal region of KLF5 (aa 1–238). Phosphorylation at a PKC site within the CBP-interaction domain of KLF5 is required for full transactivation, as shown by kinase inhibitors and site-directed mutagenesis, and phosphorylation of KLF5 enhances its interaction with CBP in GST pulldown assays. The HAT activity of CBP does not acetylate KLF5 in vitro. GAL4 fusion transactivation assay, co-immunoprecipitation, GST pulldown, site-directed mutagenesis (PKC phosphorylation site), pharmacological kinase inhibition (H7, calphostin C) Nucleic acids research High 12682370
2003 KLF5 binds the TCR Dbeta1 promoter GC-rich motifs and transactivates Dbeta1 germline transcription in pro-T cells; antibody supershift and chromatin immunoprecipitation confirmed endogenous KLF5 occupancy at the Dbeta1 promoter; a dominant-negative KLF5 construct inhibited reporter expression. Yeast one-hybrid screening, antibody supershift EMSA, chromatin immunoprecipitation (ChIP), luciferase reporter assay with dominant-negative construct Blood High 12576331
2004 In non-transformed intestinal epithelial cells, KLF5 enhances cyclin D1 transcription and promotes cell growth; however, Ras-mediated transformation switches KLF5 function so that it reduces colony formation and no longer enhances cyclin D1 transcription, demonstrating context-dependent altered function during tumor progression. KLF5 protein is destabilized in transformed cells. Stable retroviral expression, colony formation assay, cyclin D1 luciferase reporter, Ras transformation model, protein stability analysis The Journal of biological chemistry Medium 14726538
2011 TAZ stabilizes KLF5 protein by antagonizing WWP1-mediated ubiquitination; TAZ interacts with the PY motif of KLF5 through its WW domain, competing with the E3 ubiquitin ligase WWP1 for the same binding site, thereby inhibiting WWP1-mediated KLF5 ubiquitination and proteasomal degradation. This was shown to require the WW domain of TAZ and promotes breast cell proliferation. Co-immunoprecipitation, ubiquitination assay, WW-domain mutant TAZ overexpression, siRNA knockdown, xenograft tumor model Carcinogenesis High 22045023
2012 YAP interacts with KLF5 through its WW domains binding the PY motif of KLF5, preventing WWP1 E3 ligase from ubiquitinating KLF5, thereby stabilizing KLF5 protein and upregulating KLF5 target genes (FGFBP1/FGF-BP and ITGB2). LATS1 (upstream kinase of YAP) suppresses the KLF5-FGF-BP axis through YAP. Co-immunoprecipitation, WW-domain mutant YAP overexpression, siRNA knockdown, xenograft tumor model, target gene expression analysis The American journal of pathology High 22632819
2014 FBW7 (FBXW7/CDC4) is an E3 ubiquitin ligase that targets KLF5 for ubiquitination and proteasomal degradation; KLF5 contains functional Cdc4 phospho-degrons (CPDs) required for FBW7 interaction; GSK3β phosphorylates these CPDs, and mutation of CPDs blocks FBW7-mediated ubiquitination and degradation of KLF5. Ubiquitination assay, co-immunoprecipitation, site-directed mutagenesis of phospho-degrons, GSK3β kinase involvement, cancer cell line and mouse model analysis World journal of biological chemistry Medium 24921010
2015 BAP1 is a deubiquitinase (DUB) for KLF5; BAP1 directly interacts with KLF5 and stabilizes it via deubiquitination. KLF5 is present in the BAP1/HCF-1 complex. BAP1 knockdown inhibits tumorigenicity and lung metastasis, which is partially rescued by ectopic KLF5 expression. Identified by genome-wide siRNA DUB library screen. Genome-wide siRNA library screen, co-immunoprecipitation, deubiquitination assay, BAP1 knockdown with KLF5 rescue, xenograft/metastasis model Nature communications High 26419610
2015 Cardiac myocyte KLF5 directly activates PPARα (Ppara) gene expression by binding its promoter; cardiac myocyte-specific Klf5 knockout mice showed reduced Ppara expression, reduced fatty acid oxidation, decreased ATP, increased triglyceride accumulation, and cardiac dysfunction. In septic hearts, c-Jun competes with KLF5 at an overlapping site on the Ppara promoter to repress transcription. Cardiac myocyte-specific knockout mouse, ChIP (KLF5 promoter binding), luciferase reporter assay, metabolic assays (FAO, ATP), co-IP or competitor binding analysis Circulation research High 26574507
2017 In macrophages, KLF5 promotes podosome formation and cell migration by directly activating transcription of Myo9b (myosin IXB) through binding its promoter; KLF5 acts upstream of RhoA signaling (KLF5 knockdown increased RhoA-GTP levels); myeloid-specific Klf5 knockout mice showed impaired macrophage infiltration and reduced AAA formation. Myeloid-specific Klf5 knockout mice, luciferase reporter assay (Myo9b promoter), co-immunostaining, time-lapse migration imaging, RhoA-GTP pulldown assay Circulation research High 28115390
2018 HDAC1/2 deacetylate KLF5 at K369 and promote its proteasomal degradation; the deacetylase activity of HDAC1/2 is required for KLF5 degradation. An acetylation-mimicking K369Q mutation of KLF5 prevents its proteasomal degradation even though it does not affect HDAC1/2 binding. Maintaining KLF5 in a deacetylated state promotes cell proliferation. siRNA knockdown of HDAC1/2, site-directed mutagenesis (K369Q, K369R), cycloheximide chase/protein stability assay, co-immunoprecipitation Biochemical and biophysical research communications Medium 29679567
2019 USP3 is a deubiquitinase for KLF5; USP3 interacts with KLF5 and stabilizes it via deubiquitination; USP3 knockdown inhibits breast cancer cell proliferation and tumorigenesis, which is partially rescued by ectopic KLF5 expression. Identified by genome-wide siRNA DUB library screening. Genome-wide siRNA DUB library screen, co-immunoprecipitation, deubiquitination assay, USP3 knockdown with KLF5 rescue, in vivo tumorigenesis model The Journal of biological chemistry High 31624151
2020 KLF5 directly binds the promoter of NOX4 (NADPH oxidase 4) to activate its transcription; FOXO1 binds directly to the KLF5 promoter to increase KLF5 expression in diabetic cardiomyocytes; KLF5-induced NOX4 upregulation causes oxidative stress and ceramide accumulation leading to diabetic cardiomyopathy; cardiomyocyte-specific FOXO1 deletion reduced KLF5, and AAV-mediated KLF5 re-expression abolished this protection. ChIP (FOXO1 on KLF5 promoter; KLF5 on NOX4 promoter), cardiomyocyte-specific FOXO1 knockout mice, AAV-mediated KLF5 overexpression/rescue, pharmacological KLF5 inhibition, ROS/ceramide measurement Circulation research High 33539225
2020 Klf5 down-regulation in vascular smooth muscle cells leads to mitochondrial fission and vascular senescence; mechanistically, Klf5 directly activates eIF5a transcription by binding its promoter, and eIF5a in turn preserves mitochondrial integrity by interacting with mitofusin 1 (Mfn1). VSMC-specific Klf5 knockout mice showed exacerbated vascular senescence and AAA progression. VSMC-specific Klf5 knockout mice, ChIP (Klf5 binding to eIF5a promoter), co-immunoprecipitation (eIF5a–Mfn1 interaction), ROS measurement, mitochondrial imaging PLoS biology High 32817651
2020 Acetylated KLF5 (at K369) is the predominant form in basal prostate cells and is essential for proper luminal differentiation from basal progenitors; deacetylation of Klf5 (K369R knock-in) causes excess basal-to-luminal differentiation and activates Notch signaling; acetylated Klf5 maintains basal progenitors and coordinates postnatal prostate development. Acetylation-specific KLF5 K369R knock-in mouse, organoid assay, Notch signaling readout, cell lineage tracing, Western blot with acetylation-specific antibody Nature communications High 32081850
2020 KLF5 is a transcriptional regulator of skeletal muscle atrophy; KLF5 is up-regulated early in atrophying myotubes and skeletal muscle-selective Klf5 deletion attenuates mechanical unloading-induced atrophy in mice. KLF5 regulates atrophy-related metabolic and E3-ubiquitin ligase programs in coordination with Foxo1; the RAR agonist Am80 inhibits KLF5 and suppresses muscle atrophy. Skeletal muscle-specific Klf5 knockout mice, transcriptome profiling, chromatin accessibility analysis (ATAC-seq), pharmacological inhibition with Am80 (RAR agonist/KLF5 inhibitor), dexamethasone and simulated microgravity atrophy models Proceedings of the National Academy of Sciences of the United States of America High 34426497
2021 PRMT5 interacts with KLF5 and catalyzes di-methylation of KLF5 at Arginine 57 (R57) in a methyltransferase-activity-dependent manner; PRMT5-induced KLF5 R57me2 antagonizes GSK3β-mediated KLF5 phosphorylation and subsequently Fbw7-mediated ubiquitination and degradation, thereby stabilizing KLF5 and promoting breast cancer stem cell maintenance and proliferation. Co-immunoprecipitation, in vitro methylation assay, site-directed mutagenesis (R57), phosphorylation and ubiquitination assays, PRMT5 inhibitor (PJ-68), xenograft model Cell death and differentiation High 33972717
2021 KLF5 and AR physically interact on chromatin in prostate cancer cells and drive opposing transcriptional programs; KLF5 promotes cellular migration, anchorage-independent growth, and basal epithelial phenotypes while antagonizing AR activity. ERBB2 is identified as a point of transcriptional convergence activated by KLF5 and repressed by AR. Co-immunoprecipitation on chromatin, ChIP-seq, RNA-seq, gain- and loss-of-function (KLF5 overexpression/knockdown), ERBB2 inhibitor treatment Nature communications High 34737261
2021 YB-1 enhances KLF5 expression by: (1) transcriptional activation that can be inhibited by DACH1, and (2) stabilizing KLF5 mRNA in an RNA 5-methylcytosine modification-dependent manner. RSK2-mediated YB-1 phosphorylation at Ser102 promotes YB-1/KLF5 transcriptional complex formation, which co-regulates KRT16 and Ly6D expression to promote basal-like breast cancer cell proliferation. Co-immunoprecipitation, mRNA stability assay, site-directed mutagenesis (YB-1 Ser102), ChIP, luciferase reporter, RSK inhibitor (LJH685) in vivo Cell death and differentiation Medium 35022570
2021 KLF5 directly binds the promoter of COX2 and promotes its transcription; KLF5 deficiency decreases PGE2 release from tumor cells by reducing COX2 expression, thereby increasing CD8+ T-cell infiltration and function in the tumor microenvironment; inhibition of the KLF5/COX2 axis synergizes with anti-PD1 therapy. ChIP (KLF5 on COX2 promoter), luciferase reporter assay, RNA-seq, KLF5 knockout/overexpression in tumor cells, flow cytometry (T-cell infiltration), mouse tumor models Theranostics Medium 36923542
2021 Klf5 establishes bi-potential cell fate in early mouse embryos by dual regulation: Klf5 directly induces both ICM specification genes and TE specification genes; Klf5 acts redundantly with Klf4 during ICM specification but Klf5 alone is required for TE specification. Klf5 is regulated by the 2C-specific factor Dux, and the Dux/Klf5 axis is evolutionarily conserved. ChIP-seq (direct target identification), Klf5 knockout embryos, chimeric embryo assay with Klf5-overexpressing ESCs, genetic epistasis (Klf5/Klf4 double mutant) Cell reports High 34758315
2022 WWP2 monoubiquitinates KLF5 via its catalytic Cys838; monoubiquitination (not polyubiquitination/degradation) of KLF5 by WWP2 transactivates KLF5, promoting expression of downstream odontoblast differentiation genes Dmp1 and Dspp. WWP2 interaction requires the PY2 motif (PPPSY) of KLF5. Lysine residues K31, K52, K83, and K265 of KLF5 are essential for WWP2-mediated transactivation. Co-immunoprecipitation, ubiquitination assay (K48-linkage analysis), site-directed mutagenesis (WWP2 C838A, KLF5 PY2 motif, KLF5 lysine residues), siRNA knockdown, ALP/Alizarin Red differentiation assays Journal of dental research High 33164644
2022 HDACi (SAHA, TSA) increase KLF5 acetylation at K369 and promote its proteasomal degradation via ubiquitination; K369 acetylation decreases binding of KLF5 to its deubiquitinase BAP1, thus reducing KLF5 stability. This reveals a crosstalk between KLF5 acetylation (K369) and its ubiquitination/stability. Western blot with acetylation-specific antibody, ubiquitination assay, co-immunoprecipitation (KLF5–BAP1 interaction with K369 mutants), SAHA/TSA treatment, site-directed mutagenesis (K369) International journal of biological sciences Medium 35342356
2022 Klf5 is an essential determinant of AT1 alveolar epithelial cell lineage fidelity during lung development; Klf5 represses AT2 cell proliferation and enhances AT2-to-AT1 cell differentiation in a spatially restricted manner during lung regeneration; Klf5 reduces AT2 cell sensitivity to inflammatory signaling to drive AT2-AT1 differentiation, as shown in infectious and non-infectious ARDS models. Cell-type-specific Klf5 conditional knockout mice, organoid assay, transcriptomic and epigenetic profiling, lung injury models (ARDS) Developmental cell High 35803279
2022 α-Catulin interacts with the C-terminal region of KLF5 and inhibits WWP1-mediated degradation of KLF5, thereby stabilizing KLF5 and promoting cancer stem-like properties in non-small cell lung cancer; ILK inhibition disrupts the α-Catulin–KLF5 interaction and promotes KLF5 degradation. Yeast two-hybrid, co-immunoprecipitation, cycloheximide chase assay, ILK inhibitor treatment, sphere formation and xenograft assays Theranostics Medium 35154481
2023 SRC kinase-mediated tyrosine phosphorylation of YAP1 induces YAP1 interaction with KLF5 to form a YAP1/TEAD-KLF5 transcriptional complex; this complex promotes TEAD-mediated transcription independently of canonical Hippo kinases, driving cancer stemness and metastasis in TNBC. Co-immunoprecipitation, SRC inhibition, phospho-YAP1 mutant analysis, transcriptomic and proteomic analysis, TNBC xenograft and metastasis models Cellular and molecular life sciences : CMLS Medium 36633714
2023 KLF5 forms a transcriptional complex with EHF and ELF3 and binds to the promoter region of RAD51 to enhance its transcription, strengthening the homologous recombination repair (HRR) pathway; super-enhancers drive relative cancer-specific expression of KLF5 in ovarian cancer. ChIP (KLF5 on RAD51 promoter), co-immunoprecipitation (KLF5–EHF–ELF3 complex), super-enhancer analysis, luciferase reporter, functional HRR assay Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 37702443
2023 PRMT5 interacts with KLF5 and catalyzes dimethylation of KLF5 at Arginine 41 in lung cancer cells in a methyltransferase-activity-dependent manner; this methylation stabilizes KLF5 by promoting the Akt/GSK3β signaling axis, and PRMT5 depletion/inhibition reduces KLF5 expression and downstream targets. Co-immunoprecipitation, in vitro methylation assay, PRMT5 inhibitor treatment, Akt/GSK3β pathway analysis, siRNA knockdown, in vivo tumor model Journal of cellular and molecular medicine Medium 37461162
2024 PTEN deficiency induces KLF5 acetylation; deacetylated KLF5 in prostate cancer cells promotes secretion of TNF-α, which stimulates cancer-associated fibroblasts (CAFs) to release FGF9; FGF9 activates FGFR1 signaling in cancer cells, enhancing tumor growth; CX3CR1 inhibition blocked FGFR1 activation and sensitized PTEN-deficient prostate cancer to AKT inhibitor capivasertib. Klf5 acetylation knock-in mouse, co-culture assays (cancer cell–CAF interaction), cytokine ELISA, FGFR1 signaling analysis, pharmacological inhibition (CX3CR1 inhibitor + AKT inhibitor) The Journal of clinical investigation Medium 38781024
2024 Histone H3 lysine 14 lactylation (H3K14la), driven by elevated lactate in diabetic kidney disease, facilitates KLF5 expression at the chromatin level; KLF5 then binds the cdh1 (E-cadherin) promoter and inhibits its transcription, accelerating epithelial-mesenchymal transition. ChIP-seq revealed H3K14la at the KLF5 locus and RNA-seq linked this to EMT gene programs. ChIP-seq (H3K14la at KLF5 locus), RNA-seq, ChIP (KLF5 binding to cdh1 promoter), lactate reduction experiments, nephron-specific KLF5 knockdown mouse, KLF5 inhibitor (ML264) Redox biology Medium 38925041
2018 KLF5 deacetylation (by HDAC1/2) is linked to its proteasomal degradation: silencing HDAC1/2 upregulates KLF5 protein without affecting mRNA, through reduced proteasomal degradation. An acetylation-mimicking K369Q mutation prevents KLF5 degradation, while a K369R mutation (blocks acetylation) does not affect HDAC1/2 binding or KLF5 degradation response. siRNA knockdown, cycloheximide chase, proteasome inhibitor MG132, site-directed mutagenesis (K369Q, K369R), co-immunoprecipitation Biochemical and biophysical research communications Medium 29679567
2018 KLF5 promotes cell migration and lamellipodia formation in bladder cancer by transcriptionally activating FYN through direct binding to the FYN promoter; KLF5 overexpression increases FYN expression and FAK phosphorylation; FYN overexpression rescues migration reduced by KLF5 knockdown, placing KLF5 upstream of FYN in a KLF5/FYN/p-FAK migration axis. ChIP (KLF5 on FYN promoter), luciferase reporter assay, siRNA knockdown, FYN rescue experiment, lamellipodia imaging FEBS letters Medium 26786295
2020 In cancer chromatin, KLF5 interacts with TP63 and YAP1 transcription factors and with the CBP/EP300 acetyltransferase complex; KLF5 guides the CBP/EP300 complex to increase H3K27 acetylation, which enhances BRD4 recruitment; 3D chromatin looping (HiChIP) aggregates multiple distal KLF5 binding events to synergistically activate individual target genes and drive RNA Pol II elongation. HiChIP (3D chromatin architecture), immunoprecipitation-mass spectrometry (KLF5 interactome), ChIP-seq (H3K27ac, BRD4), PROTAC-mediated BRD4 degradation, KLF5 dependency screen Cancer research High 33115806
2021 KLF5 is indispensable for maintaining basal progenitors in the intestinal stem cell niche; inducible deletion of Klf5 in Lgr5+ stem cells suppressed their proliferation and survival, associated with nuclear β-catenin localization and abnormal apoptosis; oncogenic β-catenin-driven adenoma/carcinoma production in Lgr5+ cells was completely suppressed by Klf5 deletion in the same cells, placing KLF5 downstream of or required for Wnt/β-catenin oncogenesis. Inducible Lgr5-specific Klf5 knockout mice, β-catenin nuclear localization analysis, oncogenic β-catenin knock-in crossed with Klf5 deletion, histological analysis of adenoma/carcinoma formation Cancer research High 24626089
2018 Klf5 suppresses ERK signaling in mouse embryonic stem cells; Klf5-knockout ESCs showed over-activated ERK, reintroduction of Klf5 (but not Klf2 or Klf4) suppressed ERK. Klf5 regulates Spred1, a negative regulator of the FGF-ERK pathway, providing a molecular mechanism for ERK suppression. Klf5-KO ESC lines, ERK phosphorylation analysis, Klf5 re-expression (specificity comparison with Klf2, Klf4), Spred1 expression analysis, EpiSC reprogramming assay PloS one Medium 30452437
2014 Simultaneous knockdown of KLF5 and Fli1 in dermal fibroblasts synergistically enhances connective tissue growth factor expression; double heterozygous Klf5/Fli1 mice spontaneously develop all three cardinal features of systemic sclerosis (fibrosis, vasculopathy, autoantibody production), establishing epigenetic co-downregulation of these two transcription factors as a central pathogenic event. siRNA double knockdown in primary fibroblasts, Klf5+/- Fli1+/- double heterozygous mouse model, histological/immunological phenotyping Nature communications High 25504335

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Krüppel-like zinc-finger transcription factor KLF5/BTEB2 is a target for angiotensin II signaling and an essential regulator of cardiovascular remodeling. Nature medicine 334 12101409
2009 Essential role of KLF5 transcription factor in cell proliferation and differentiation and its implications for human diseases. Cellular and molecular life sciences : CMLS 231 19448973
2015 BAP1 promotes breast cancer cell proliferation and metastasis by deubiquitinating KLF5. Nature communications 180 26419610
1993 cDNA cloning and transcriptional properties of a novel GC box-binding protein, BTEB2. Nucleic acids research 180 8479902
2005 KLF4 and KLF5 regulate proliferation, apoptosis and invasion in esophageal cancer cells. Cancer biology & therapy 164 16357509
2006 KLF5 promotes cell proliferation and tumorigenesis through gene regulation and the TSU-Pr1 human bladder cancer cell line. International journal of cancer 131 16184550
2020 KLF5 Is Induced by FOXO1 and Causes Oxidative Stress and Diabetic Cardiomyopathy. Circulation research 126 33539225
1999 BTEB2, a Krüppel-like transcription factor, regulates expression of the SMemb/Nonmuscle myosin heavy chain B (SMemb/NMHC-B) gene. Circulation research 117 10417400
2024 Lactate drives epithelial-mesenchymal transition in diabetic kidney disease via the H3K14la/KLF5 pathway. Redox biology 116 38925041
2014 Simultaneous downregulation of KLF5 and Fli1 is a key feature underlying systemic sclerosis. Nature communications 115 25504335
2012 YAP promotes breast cell proliferation and survival partially through stabilizing the KLF5 transcription factor. The American journal of pathology 114 22632819
2021 The roles and regulation of the KLF5 transcription factor in cancers. Cancer science 112 33811715
2004 Intestinal tumor progression is associated with altered function of KLF5. The Journal of biological chemistry 106 14726538
2015 Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function. Circulation research 101 26574507
2014 Klf4 and Klf5 differentially inhibit mesoderm and endoderm differentiation in embryonic stem cells. Nature communications 99 24770696
2005 Significance of the transcription factor KLF5 in cardiovascular remodeling. Journal of thrombosis and haemostasis : JTH 86 16102021
2011 TAZ antagonizes the WWP1-mediated KLF5 degradation and promotes breast cell proliferation and tumorigenesis. Carcinogenesis 81 22045023
1999 Transcriptional activation of the zinc finger transcription factor BTEB2 gene by Egr-1 through mitogen-activated protein kinase pathways in vascular smooth muscle cells. Circulation research 78 10532946
2000 Developmental expression of the mouse gene coding for the Krüppel-like transcription factor KLF5. Developmental dynamics : an official publication of the American Association of Anatomists 71 10767086
2015 Targeting Krüppel-like factor 5 (KLF5) for cancer therapy. Current topics in medicinal chemistry 69 25732792
2014 KLF5 regulates the integrity and oncogenicity of intestinal stem cells. Cancer research 69 24626089
2003 Phosphorylation of Kruppel-like factor 5 (KLF5/IKLF) at the CBP interaction region enhances its transactivation function. Nucleic acids research 67 12682370
2022 YB-1 is a positive regulator of KLF5 transcription factor in basal-like breast cancer. Cell death and differentiation 65 35022570
2020 Klf5 down-regulation induces vascular senescence through eIF5a depletion and mitochondrial fission. PLoS biology 65 32817651
1999 Isolation and characterization of a gene encoding human Kruppel-like factor 5 (IKLF): binding to the CAAT/GT box of the mouse lactoferrin gene promoter. Nucleic acids research 61 10572182
2018 Cholesterol promotes the migration and invasion of renal carcinoma cells by regulating the KLF5/miR-27a/FBXW7 pathway. Biochemical and biophysical research communications 60 29782853
2001 Identification of a mouse homolog of the human BTEB2 transcription factor as a beta-catenin-independent Wnt-1-responsive gene. Molecular and cellular biology 57 11134343
2019 USP3 promotes breast cancer cell proliferation by deubiquitinating KLF5. The Journal of biological chemistry 56 31624151
2015 KLF5 mediates vascular remodeling via HIF-1α in hypoxic pulmonary hypertension. American journal of physiology. Lung cellular and molecular physiology 55 26702149
2021 Arginine methyltransferase PRMT5 methylates and stabilizes KLF5 via decreasing its phosphorylation and ubiquitination to promote basal-like breast cancer. Cell death and differentiation 54 33972717
2018 miR-21 promotes cell migration and invasion of hepatocellular carcinoma by targeting KLF5. Oncology letters 52 30675287
2014 KLF5 promotes hypoxia-induced survival and inhibits apoptosis in non-small cell lung cancer cells via HIF-1α. International journal of oncology 50 25051115
2017 Inhibition of KLF5-Myo9b-RhoA Pathway-Mediated Podosome Formation in Macrophages Ameliorates Abdominal Aortic Aneurysm. Circulation research 48 28115390
2021 YAP regulates alveolar epithelial cell differentiation and AGER via NFIB/KLF5/NKX2-1. iScience 46 34466790
2013 The double life of KLF5: Opposing roles in regulation of gene-expression, cellular function, and transformation. IUBMB life 45 24323942
2020 Chromatin Looping Shapes KLF5-Dependent Transcriptional Programs in Human Epithelial Cancers. Cancer research 42 33115806
2017 miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5. PloS one 41 28437471
2023 KLF5 Promotes Tumor Progression and Parp Inhibitor Resistance in Ovarian Cancer. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 38 37702443
2019 Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers. International journal of biological sciences 38 31360115
2021 Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health. Journal of molecular and cellular cardiology 37 34653523
2019 EGFR and Prion protein promote signaling via FOXO3a-KLF5 resulting in clinical resistance to platinum agents in colorectal cancer. Molecular oncology 35 30478887
2009 Spatial and temporal expression of KLF4 and KLF5 during murine tooth development. Archives of oral biology 35 19268913
2021 Identification of a KLF5-dependent program and drug development for skeletal muscle atrophy. Proceedings of the National Academy of Sciences of the United States of America 33 34426497
2021 Opposing transcriptional programs of KLF5 and AR emerge during therapy for advanced prostate cancer. Nature communications 33 34737261
2020 Klf5 acetylation regulates luminal differentiation of basal progenitors in prostate development and regeneration. Nature communications 33 32081850
2021 Klf5 establishes bi-potential cell fate by dual regulation of ICM and TE specification genes. Cell reports 32 34758315
2019 Excessive miR-152-3p Results in Increased BAFF Expression in SLE B-Cells by Inhibiting the KLF5 Expression. Frontiers in immunology 31 31178864
2015 KLF5 regulates infection- and inflammation-induced pro-labour mediators in human myometrium. Reproduction (Cambridge, England) 31 25687411
1997 Transcriptional activation domain of human BTEB2, a GC box-binding factor. Journal of biochemistry 31 9089417
2023 KLF5 inhibition potentiates anti-PD1 efficacy by enhancing CD8+ T-cell-dependent antitumor immunity. Theranostics 30 36923542
2020 Long intergenic noncoding RNA 00908 promotes proliferation and inhibits apoptosis of colorectal cancer cells by regulating KLF5 expression. Journal of cellular physiology 30 33020901
2003 Regulation of T-cell receptor D beta 1 promoter by KLF5 through reiterated GC-rich motifs. Blood 30 12576331
2016 KLF5 promotes cell migration by up-regulating FYN in bladder cancer cells. FEBS letters 29 26786295
2014 CEBPA-dependent HK3 and KLF5 expression in primary AML and during AML differentiation. Scientific reports 29 24584857
2003 KLF5/BTEB2, a Krüppel-like zinc-finger type transcription factor, mediates both smooth muscle cell activation and cardiac hypertrophy. Advances in experimental medicine and biology 29 15098654
2021 KLF5-induced lncRNA IGFL2-AS1 promotes basal-like breast cancer cell growth and survival by upregulating the expression of IGFL1. Cancer letters 28 34052325
2021 KLF5/LINC00346/miR‑148a‑3p axis regulates inflammation and endothelial cell injury in atherosclerosis. International journal of molecular medicine 28 34165154
2017 Regulatory crosstalk between KLF5, miR-29a and Fbw7/CDC4 cooperatively promotes atherosclerotic development. Biochimica et biophysica acta. Molecular basis of disease 28 29074464
2024 Acetyl-CoA synthetase 2 induces pyroptosis and inflammation of renal epithelial tubular cells in sepsis-induced acute kidney injury by upregulating the KLF5/NF-κB pathway. Cell communication and signaling : CCS 26 38515158
2021 BAP1 antagonizes WWP1-mediated transcription factor KLF5 ubiquitination and inhibits autophagy to promote melanoma progression. Experimental cell research 25 33516665
2023 Tyrosine kinase SRC-induced YAP1-KLF5 module regulates cancer stemness and metastasis in triple-negative breast cancer. Cellular and molecular life sciences : CMLS 24 36633714
2022 Histone Deacetylase Inhibitors (HDACi) Promote KLF5 Ubiquitination and Degradation in Basal-like Breast Cancer. International journal of biological sciences 24 35342356
2022 Klf5 defines alveolar epithelial type 1 cell lineage commitment during lung development and regeneration. Developmental cell 24 35803279
2023 Targeting the KLF5-EphA2 axis can restrain cancer stemness and overcome chemoresistance in basal-like breast cancer. International journal of biological sciences 23 37063424
2020 KLF5 promotes proliferation in gastric cancer via regulating p21 and CDK4. European review for medical and pharmacological sciences 22 32373958
2019 MKK7 transcription positively or negatively regulated by SP1 and KLF5 depends on HDAC4 activity in glioma. International journal of cancer 22 30963560
2018 KLF5 promotes the tumorigenesis and metastatic potential of thyroid cancer cells through the NF-κB signaling pathway. Oncology reports 22 30226614
2022 α-Catulin promotes cancer stemness by antagonizing WWP1-mediated KLF5 degradation in lung cancer. Theranostics 20 35154481
2021 KLF5 and NFYA factors as novel regulators of prostate cancer cell metabolism. Endocrine-related cancer 20 33690159
2021 A Positive Feedback Loop of Long Noncoding RNA LINC00152 and KLF5 Facilitates Breast Cancer Growth. Frontiers in oncology 20 33842324
2021 KLF5 activates lncRNA DANCR and inhibits cancer cell autophagy accelerating gastric cancer progression. NPJ genomic medicine 20 34548487
2020 WWP2 Promotes Odontoblastic Differentiation by Monoubiquitinating KLF5. Journal of dental research 20 33164644
2019 CDX1/2 and KLF5 Expression and Epigenetic Modulation of Sonic Hedgehog Signaling in Gastric Adenocarcinoma. Pathology oncology research : POR 20 30685841
2018 miR-448-3p controls intracranial aneurysm by regulating KLF5 expression. Biochemical and biophysical research communications 20 30322616
2015 The transient expression of Klf4 and Klf5 during adipogenesis depends on GSK3β activity. Adipocyte 20 26451280
2025 Porphyromonas gingivalis potentiates stem-like properties of oral squamous cell carcinoma by modulating SCD1-dependent lipid synthesis via NOD1/KLF5 axis. International journal of oral science 19 40016182
2024 Interruption of KLF5 acetylation promotes PTEN-deficient prostate cancer progression by reprogramming cancer-associated fibroblasts. The Journal of clinical investigation 19 38781024
2023 Nitazoxanide inhibits acetylated KLF5-induced bone metastasis by modulating KLF5 function in prostate cancer. BMC medicine 19 36810084
2021 Interfering microRNA-410 attenuates atherosclerosis via the HDAC1/KLF5/IKBα/NF-κB axis. Molecular therapy. Nucleic acids 19 33981482
2021 MicroRNA-146a-3p/HDAC1/KLF5/IKBα signal axis modulates plaque formation of atherosclerosis mice. Life sciences 19 34004248
2021 LINC01123 promotes cell proliferation and migration via regulating miR-1277-5p/KLF5 axis in ox-LDL-induced vascular smooth muscle cells. Journal of molecular histology 19 34403009
2018 HDAC-mediated deacetylation of KLF5 associates with its proteasomal degradation. Biochemical and biophysical research communications 19 29679567
2018 miR‑590‑5p suppresses osteosarcoma cell proliferation and invasion via targeting KLF5. Molecular medicine reports 19 29916536
2021 KLF5-mediated Eppk1 expression promotes cell proliferation in cervical cancer via the p38 signaling pathway. BMC cancer 18 33827480
2021 KLF5 Is Activated by Gene Amplification in Gastric Cancer and Is Essential for Gastric Cell Proliferation. Cells 18 33923166
2021 CircATRNL1 protects against osteoarthritis by targeting miR-153-3p and KLF5. International immunopharmacology 18 33971492
2021 The Partial Role of KLF4 and KLF5 in Gastrointestinal Tumors. Gastroenterology research and practice 18 34367275
2020 KLF5 regulates chicken skeletal muscle atrophy via the canonical Wnt/β-catenin signaling pathway. Experimental animals 18 32641593
2020 BTEB2-Activated lncRNA TSPEAR-AS2 Drives GC Progression through Suppressing GJA1 Expression and Upregulating CLDN4 Expression. Molecular therapy. Nucleic acids 18 33294297
2019 Hyperinsulinemia-induced KLF5 mediates endothelial angiogenic dysfunction in diabetic endothelial cells. Journal of molecular histology 17 31049798
2003 Smooth muscle cell outgrowth from coronary atherectomy specimens in vitro is associated with less time to restenosis and expression of a key Transcription factor KLF5/BTEB2. Cardiology 17 14557694
2021 RNA-seq analysis reveals the positive role of KLF5 in the differentiation of subcutaneous adipocyte in goats. Gene 16 34530084
2019 Identification and functional characterization of KLF5 as a novel disease gene responsible for familial dilated cardiomyopathy. European journal of medical genetics 16 31857253
2018 Overexpression of KLF5 inhibits puromycin‑induced apoptosis of podocytes. Molecular medicine reports 16 30106142
2018 Klf5 suppresses ERK signaling in mouse pluripotent stem cells. PloS one 16 30452437
2024 Activation of the YAP/KLF5 transcriptional cascade in renal tubular cells aggravates kidney injury. Molecular therapy : the journal of the American Society of Gene Therapy 15 38414248
2021 MicroRNA-140-3p alleviates intervertebral disc degeneration via KLF5/N-cadherin/MDM2/Slug axis. RNA biology 15 33904383
2014 FBW7-mediated ubiquitination and degradation of KLF5. World journal of biological chemistry 15 24921010
2023 PRMT5 activates KLF5 by methylation to facilitate lung cancer. Journal of cellular and molecular medicine 14 37461162
2021 BAP1 promotes viability and migration of ECA109 cells through KLF5/CyclinD1/FGF-BP1. FEBS open bio 14 33529461

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