| 2001 |
KLF13 (BTEB3) contains a direct repressor domain in its N-terminus that interacts with co-repressor mSin3A and histone deacetylase HDAC-1, and mediates repression also by competing with Sp1 for binding to GC-rich BTE DNA elements. |
Immunoprecipitation, GAL4 fusion assays, gel shift assays, reporter assays in CHO cells |
The Journal of biological chemistry |
High |
11477107
|
| 2002 |
KLF13 (RFLAT-1) has distinct N-terminal transcriptional activation (aa 1-35) and repression (aa 67-168) domains; contains two independent nuclear localization signals (one upstream of and one within the zinc fingers); binds the critical CTCCC sequence on the RANTES promoter; and synergizes with NF-κB for RANTES transcription. |
GAL4 fusion system, deletion analysis, site-directed mutagenesis, GFP fusion NLS mapping, gel shift/mutational analysis, reporter assays |
The Journal of biological chemistry |
High |
12050170
|
| 2002 |
KLF13 (RFLAT-1) protein expression is translationally regulated through its 5'-UTR in a cell-type-specific manner via cap-dependent translation involving eIF4E and its kinase Mnk1, downstream of ERK-1/2 and p38 MAP kinases. |
Overexpression of eIF4E, Mnk1 inhibition, kinase pathway inhibitors, quantitative PCR and protein analysis |
The Journal of clinical investigation |
High |
12093895
|
| 2003 |
CBP and PCAF co-activators acetylate KLF13 at specific lysine residues in its zinc finger domain; CBP acetylation disrupts KLF13 DNA binding, while PCAF blocks CBP-mediated acetylation to prevent this disruption, and CBP acetylation of KLF13 prevents PCAF stimulation of KLF13 DNA binding—demonstrating antagonistic and synergistic functional interplay between the two acetyltransferases. |
In vitro acetylation assays, gel shift assays, site-directed mutagenesis, co-activator co-expression reporter assays |
Journal of molecular biology |
High |
12758070
|
| 2003 |
KLF13 (BTEB3) binds to TGGG repeat motifs in the SM22α promoter and activates or inhibits reporter gene expression depending on which TGGG box it occupies; only one of three boxes is required for BTEB3-dependent activation in P19 cells; KLF13 activates the SM22α promoter in vascular smooth muscle cells (VSMCs) and is expressed in VSMCs in vitro with modulated expression after injury in vivo. |
Recombinant protein binding assays, mutation analysis, transient transfection reporter assays in P19 and VSMC cells |
The Biochemical journal |
Medium |
12848620
|
| 2005 |
KLF13 represses the low density lipoprotein receptor (LDLR) promoter by binding proximal LDLR DNA sequences in vivo (confirmed by ChIP) in a DNA context-selective manner; this repression is antagonized by Sp1 and SREBP, and KLF13 binding is upregulated by oxysterols. |
RNA interference, EMSA, ChIP, reporter assays, deletion and site-directed mutagenesis, HDAC inhibitor treatment |
The Journal of biological chemistry |
High |
16303770
|
| 2006 |
KLF13 binds conserved regulatory elements on cardiac promoters, activates cardiac transcription, and physically and functionally interacts with GATA-4 to synergistically activate cardiac gene expression; knockdown of KLF13 in Xenopus embryos causes atrial septal defects and hypotrabeculation similar to GATA-4 hypomorphs. |
Xenopus knockdown (morpholino), co-immunoprecipitation, reporter assays, in situ hybridization, promoter binding assays |
The EMBO journal |
High |
17053787
|
| 2008 |
KLF13 deficiency in mice causes accumulation of DP thymocytes, reduction of CD4+ SP cells, altered surface expression of CD3, CD8, CD5, and HSA on DP cells consistent with TCR signaling defects, impaired peripheral T cell activation, a partial block at the CD43+ to CD43− pre-B cell transition, and increased CD21/CD23 expression on peripheral B cells. |
KLF13 knockout mice, flow cytometry, cell surface marker analysis |
Cell cycle (Georgetown, Tex.) |
High |
18604172
|
| 2010 |
miR-125a directly targets the 3'-UTR of KLF13 mRNA (confirmed by luciferase reporter), negatively regulates KLF13 protein expression in a dose-dependent manner, and thereby suppresses RANTES expression in activated T cells. |
Luciferase reporter assay, gain- and loss-of-function miRNA transfection, qPCR, ELISA |
Arthritis and rheumatism |
High |
20589685
|
| 2010 |
KLF13 participates in uterine stromal cell differentiation through cross-regulation with BMP2 and KLF9: KLF13 knockdown attenuates BMP2 expression and abrogates BMP2-mediated inhibition of KLF9, while KLF13 expression is positively associated with BMP2 and inversely with KLF9. |
siRNA knockdown in human endometrial stromal cells (HESCs), recombinant BMP2 treatment, KLF9 null mice, qPCR |
Endocrinology |
Medium |
20410205
|
| 2011 |
KLF13 is required in BALB/c mice for maintenance of IL-4-generating invariant NKT (iNKT) cells; KLF13-deficient BALB/c mice have iNKT cell numbers comparable to C57BL/6 mice and extremely low levels of thymic memory-like CD8+ T cells, demonstrating that KLF13 sustains iNKT cells that produce IL-4 sufficient to drive thymic memory-like CD8+ T cell generation. |
KLF13 knockout mice (BALB/c background), flow cytometry, IL-4 neutralization, IL-4 supplementation |
The Journal of experimental medicine |
High |
21482696
|
| 2012 |
KLF13 protein is degraded in resting human T lymphocytes via GSK3β-mediated phosphorylation that triggers ubiquitination by the E3 ligase Fbw7γ; proteasomal or lysosomal inhibition stabilizes KLF13 and increases RANTES expression. This mechanism is absent in murine T cells due to lack of Fbw7γ. |
Proteasomal/lysosomal inhibitor treatment, GSK3β and Fbw7γ siRNA knockdown, protein analysis by western blot |
Blood |
High |
22797700
|
| 2014 |
KLF13 directly binds IL-4 promoter regions and synergizes with the transcription factor c-Maf to positively regulate IL-4 expression in CD4+ T cells; KLF13-deficient mice show reduced IL-4 and Th2 cytokine gene expression without changes in GATA3 or c-Maf levels. |
KLF13 knockout mice, gene expression analysis, ChIP (promoter binding), reporter/synergy assays |
Journal of immunology |
High |
24821970
|
| 2015 |
KLF13 promotes porcine adipocyte differentiation by directly binding to a KLF13-binding site within the −593/−577 region of the porcine PPARγ proximal promoter and transactivating PPARγ expression; siRNA knockdown of KLF13 attenuates porcine adipocyte differentiation. |
siRNA knockdown, KLF13 overexpression, promoter deletion and mutation analysis, luciferase reporter assay |
Cell & bioscience |
Medium |
26085920
|
| 2016 |
KLF13 is upregulated in HPV-positive keratinocytes via HPV E7 protein suppression of ubiquitin ligase FBW7; KLF13 is required for HPV productive life cycle by supporting STAT5 expression, which activates the ATM DNA damage pathway and IL-8 chemokine; neutralization of IL-8 diminishes viral genome amplification. |
shRNA knockdown, qPCR, western blot, viral genome amplification assays, IL-8 neutralization |
Oncogene |
Medium |
27041562
|
| 2017 |
KLF13 physically interacts with TBX5 via TBX5's T-domain and synergistically activates transcription of cardiac genes; disease-causing TBX5 mutations in the T-domain reduce KLF13 interaction; loss of one Klf13 allele in Tbx5 heterozygous mice significantly increases penetrance of cardiac septal defects. |
Co-immunoprecipitation, reporter synergy assays, genetic epistasis in double-heterozygous mice, mutagenesis |
Human molecular genetics |
High |
28164238
|
| 2019 |
The antibiotic clofoctol upregulates KLF13 expression through its targeted binding protein UNR (Upstream of N-ras), an RNA-binding protein; elevated KLF13 acts as a tumor suppressor to inhibit glioma stem cell proliferation and induce apoptosis. |
High-throughput drug screening, target binding protein identification, downstream gene analysis, patient-derived xenografts, colony formation and apoptosis assays |
The Journal of clinical investigation |
Medium |
31112526
|
| 2020 |
KLF13 transcriptionally inhibits HMGCS1 promoter activity (confirmed by ChIP-qPCR and luciferase assay), reducing cholesterol biosynthesis in colorectal cancer cells; KLF13 knockdown or HMGCS1 overexpression rescues proliferation, establishing KLF13→HMGCS1→cholesterol biosynthesis as the tumor-suppressive mechanism. |
ChIP-qPCR, luciferase reporter assay, siRNA knockdown, overexpression, CCK-8, colony formation, cell cycle analysis, xenograft |
Cell & bioscience |
Medium |
32523679
|
| 2023 |
KLF13 recruits a repressor complex comprising SIN3A and HDAC1 to TGF-β target gene promoters, limiting their profibrotic induction; TGF-β transiently induces KLF13 as a negative feedback loop, but persistent TGF-β signaling reduces KLF13 through FBXW7-mediated ubiquitination degradation and HDAC-dependent transcriptional inhibition. |
KLF13 global knockout mice, AAV-mediated overexpression, ChIP, Co-IP for SIN3A/HDAC1 complex, reporter assays, FBXW7 interaction studies |
Cell reports |
High |
37029927
|
| 2023 |
KLF13 directly regulates expression of JAK/STAT pathway genes (Jak1, Jak2, Jak3, Socs1) by binding their proximal promoters; KLF13 differentially modulates GH-induced JAK/STAT signaling by decreasing the STAT3 branch while enhancing STAT5 activity; GH treatment increases nuclear KLF13 content and Klf13 mRNA. |
ChIP, KLF13-deficient HT22 neuronal cells, qPCR, reporter assays, GH stimulation experiments |
International journal of molecular sciences |
Medium |
37446365
|
| 2024 |
KLF13 directly binds the SM22α promoter to suppress its expression, promoting vascular smooth muscle cell (VSMC) phenotypic dedifferentiation; KLF13 knockdown ameliorates intimal hyperplasia after carotid injury, at least partly through inactivation of p-AKT signaling. |
Bioinformatics, atherosclerotic plaque analysis (human and ApoE−/− mice), siRNA knockdown, ChIP, reporter assay, carotid injury mouse model |
Journal of cellular physiology |
Medium |
38634445
|
| 2024 |
KLF13 represses Dll4 transcription (confirmed by luciferase reporter assay), inhibiting the Dll4-Notch2 axis and thereby preventing muscle atrophy; dexamethasone inhibits KLF13 expression by suppressing MYOD1-mediated KLF13 transcriptional activation and promoting FBXW7-mediated KLF13 ubiquitination. |
Transcriptome analysis, luciferase reporter assays, KLF13 KO and overexpression in cell and mouse models, MYOD1 interaction analysis |
Journal of cachexia, sarcopenia and muscle |
Medium |
38973459
|
| 2024 |
KLF13 physically interacts with PGC-1α (confirmed by Co-IP) to regulate mitochondrial quality control in alveolar epithelial cells; KLF13 overexpression reduces LPS-induced inflammation and apoptosis, and PGC-1α knockdown reverses these protective effects. |
Co-immunoprecipitation, KLF13 overexpression, PGC-1α siRNA, MitoSOX staining, JC-1 staining, western blot |
Journal of interferon & cytokine research |
Medium |
38949897
|
| 2025 |
KLF13 directly binds the GPX4 promoter (by ChIP and dual-luciferase assay) to inhibit GPX4 transcription, thereby promoting ferroptosis in lung adenocarcinoma; overexpression of GPX4 reverses KLF13-induced ferroptosis sensitization. |
ChIP assay, dual-luciferase reporter assay, stable overexpression/knockdown cell lines, ROS detection, cytotoxicity assays, xenograft model |
BMC biology |
Medium |
40597044
|
| 2025 |
KLF13 directly binds the CES2 promoter to transcriptionally activate CES2 expression; this transcriptional activation is dependent on acetylation of KLF13 by the co-activator p300, as shown by mutagenesis and p300 inhibition; the KLF13-CES2 axis controls cellular sensitivity to irinotecan in gastric cancer. |
ChIP, dual-luciferase reporter assay, site-directed mutagenesis of acetylation sites, p300 inhibition, irinotecan sensitivity assays |
iScience |
Medium |
41438085
|
| 2025 |
FBXW5 promotes ubiquitin-mediated degradation of KLF13 (confirmed by CoIP); reduced KLF13 releases transcriptional repression of TROAP, facilitating EMT in lung adenocarcinoma; KLF13 directly represses TROAP transcription as shown by ChIP and luciferase assays. |
Co-immunoprecipitation, ChIP, dual luciferase reporter assay, siRNA/overexpression, western blot, xenograft model |
Molecular carcinogenesis |
Medium |
40696794
|
| 2025 |
KLF13 transcriptionally represses SH2B1 expression by binding its promoter, which abolishes the SH2B1-IRS1 protein interaction (confirmed by Co-IP and GST pulldown), thereby repressing PI3K/AKT-mediated glycolysis in NSCLC cells. |
ChIP, dual-luciferase reporter assay, EMSA, Co-IP, GST pulldown, glycolysis assays (OCR, ECAR), xenograft model |
Clinical and translational medicine |
Medium |
41410190
|
| 2025 |
KLF13 directly promotes GPIHBP1 transcription (confirmed by luciferase and ChIP assays), regulating triacylglyceride and free fatty acid metabolism, and promoting esophageal cancer progression through this axis. |
RNA-seq, ChIP-seq, ChIP-qPCR, luciferase assay, shRNA and overexpression recovery assays, xenograft model |
Cell death & disease |
Medium |
40450000
|
| 2025 |
KLF13 promotes HTRA1 transcription (by ChIP-seq and luciferase assays) and activates the Hedgehog signaling pathway to drive breast cancer aggressiveness and immune evasion; HTRA1 overexpression rescues the anti-tumor effects of KLF13 silencing. |
ChIP-seq, luciferase assay, RNA-seq, siRNA knockdown, overexpression, in vivo xenograft |
Breast cancer (Tokyo, Japan) |
Medium |
40555914
|
| 2025 |
KLF13 acts as a transcriptional repressor of KLF target genes in maturing neocortical neurons, functioning as part of a transcriptional 'switch' from KLF activators (Klf6, Klf7) to repressors (Klf9, Klf13) that represses shared cytoskeletal targets including Tubb2b and Dpysl3 during postnatal neuronal maturation. |
Multiplexed CRISPRi knockdown in mouse neocortical neurons, chromatin accessibility analysis, gene expression profiling |
bioRxivpreprint |
Medium |
bio_10.1101_2025.02.07.636951
|