| 1997 |
Overexpression of TIEG1/KLF10 in TGF-β-sensitive PANC1 pancreatic epithelial cells is sufficient to induce apoptosis, establishing KLF10 as a downstream effector linking TGF-β signaling to cell death. |
Stable overexpression in PANC1 cells with functional apoptosis readout |
The Journal of clinical investigation |
Medium |
9153278
|
| 1999 |
TIEG1/KLF10 contains three conserved transcriptional repressor domains (R1: 10 aa, R2: 12 aa, R3: ~80 aa) outside the zinc finger DNA-binding domain that are functionally conserved between TIEG1 and TIEG2, as defined by extensive mutagenesis and GAL4-based transcriptional assays. |
Extensive mutagenesis combined with GAL4-based transcriptional reporter assays |
The Journal of biological chemistry |
High |
10506214
|
| 1999 |
TIEG1/KLF10-induced apoptosis in Hep 3B cells proceeds via a mechanism involving increased reactive oxygen species generation and loss of mitochondrial membrane potential, preceding caspase-3 activation and glutathione depletion; the antioxidant trolox blocks both ROS and apoptosis. |
ROS measurement, mitochondrial membrane potential assay, caspase activity assay, antioxidant rescue experiment in Hep 3B cells |
Hepatology (Baltimore, Md.) |
High |
10573529
|
| 2000 |
Stable overexpression of TIEG1/KLF10 in human osteosarcoma MG-63 cells mimics TGF-β action: increased alkaline phosphatase activity, decreased osteocalcin mRNA/protein, and decreased cell proliferation, without additive effect upon TGF-β treatment. |
Stable transfection of TIEG cDNA in MG-63 cells with gene expression and proliferation assays |
The Journal of biological chemistry |
Medium |
10816551
|
| 2003 |
The zinc finger domain of TIEG1/KLF10 binds a GT-rich consensus core sequence (5'-GGTGTG-3') as established by iterative nitrocellulose filter-binding selection from a random oligonucleotide library and mutational analysis. |
In vitro selection from random oligonucleotide library (SELEX-like), nitrocellulose filter binding, mutational analysis of binding site |
DNA and cell biology |
High |
12804117
|
| 2003 |
Nitric oxide (NO) upregulates TIEG1/KLF10 mRNA in human IMR-90 fibroblasts by stabilizing the transcript (6-fold increase in half-life), independently of TGF-β, as shown by anti-TGF-β antibody blocking and mRNA half-life measurements. |
Northern blotting, anti-TGF-β antibody neutralization, mRNA stability assay |
Free radical biology & medicine |
Medium |
12788480
|
| 2004 |
TIEG1/KLF10 overexpression in oligodendroglial OLI-neu cells induces apoptosis by repressing Bcl-XL expression and enhancing SMAD-dependent TGF-β signaling, while reducing SMAD7 promoter activity. |
Overexpression in OLI-neu cells, apoptosis ELISA, DNA fragmentation, caspase-3 assay, luciferase reporter for SMAD7 promoter |
Journal of neuroscience research |
Medium |
14743447
|
| 2005 |
TIEG1/KLF10 knockout osteoblasts are defective in BMP2-induced mineralization in vitro and show decreased RANKL and increased OPG expression, resulting in impaired support of osteoclast differentiation. |
TIEG1 knockout mouse calvarial osteoblast culture, BMP2 treatment, mineralization nodule assay, osteoclast co-culture with RANKL/M-CSF rescue |
Molecular and cellular biology |
High |
15657444
|
| 2007 |
BMP2 opposes Shh-mediated proliferation in cerebellar granule neuron precursors by inducing TIEG1/KLF10, which occupies Sp1 sites in the N-myc promoter and blocks N-myc expression, leading to cell cycle arrest. |
Chromatin occupancy at Nmyc promoter, ectopic TIEG1 expression in cerebellar granule neuron precursors, cell cycle analysis |
The Journal of biological chemistry |
Medium |
17951258
|
| 2007 |
TIEG1/KLF10 induces apoptosis through the mitochondrial pathway in K562 leukemia cells, involving Bax and Bim up-regulation, Bcl-2 and Bcl-XL down-regulation, cytochrome c release, caspase-3 activation, and mitochondrial membrane potential disruption. |
TIEG1 overexpression in K562 cells, Western blotting for Bcl-2 family members, cytochrome c release assay, caspase-3 activity, mitochondrial membrane potential measurement |
FEBS letters |
Medium |
17659279
|
| 2008 |
The E3 ubiquitin ligase Itch associates with TIEG1/KLF10 and promotes its non-proteolytic K63-linked ubiquitination; this cooperates with TIEG1 to induce Foxp3 expression in T cells, and TGF-β-converted Tregs from TIEG1-deficient mice fail to suppress airway inflammation. |
Co-immunoprecipitation, ubiquitination assay, Itch-/- and TIEG1-/- mouse T cell functional studies, in vivo airway inflammation model |
Nature immunology |
High |
18278048
|
| 2008 |
KLF10 directly transactivates both the TGF-β1 and Foxp3 promoters in CD4+ T cells in response to TGF-β1, forming a positive feedback loop; KLF10-/- CD4+CD25- T cells show enhanced Th1/Th2 differentiation and cannot be suppressed by wild-type Tregs, while KLF10-/- Tregs have reduced TGF-β1 production and suppressor function rescued by exogenous TGF-β1. |
KLF10 KO mouse CD4+ T cell functional studies, promoter transactivation assays, Th1/Th2 cytokine profiling, atherosclerosis model |
The Journal of biological chemistry |
High |
19602726
|
| 2008 |
KLF10 is a VHL target gene; KLF10 transactivates the TGFBI (BIGH3) promoter as assessed by luciferase reporter assay, establishing KLF10 as an intermediate between VHL status and ECM gene expression in clear cell carcinoma. |
Expression arrays, luciferase reporter assay of TGFBI promoter with KLF10 co-transfection, cell lines with different VHL status |
Biochemical and biophysical research communications |
Medium |
18359287
|
| 2010 |
TIEG1/KLF10 directly binds the Bmal1 promoter through two juxtaposed GC boxes near the transcription initiation site and represses Bmal1 transcription; siRNA knockdown of TIEG1 causes period shortening in cellular bioluminescence rhythms driven by Bmal1-luciferase and Per2-luciferase reporters. |
In vitro transcription assay, luciferase reporter with mutational analysis, siRNA knockdown, real-time bioluminescence circadian assay |
Genes to cells : devoted to molecular & cellular mechanisms |
High |
20070857
|
| 2010 |
KLF10 displays circadian expression in mouse liver driven by CLOCK-BMAL1; the Klf10 promoter recruits BMAL1 and is transactivated by CLOCK-BMAL1 through a conserved E-box. KLF10 deficiency in liver causes postprandial/fasting hyperglycemia with upregulation of Pepck; KLF10 directly represses the Pepck promoter. |
KLF10 KO mice, Bmal1 KO mice, chromatin immunoprecipitation of BMAL1 at Klf10 promoter, liver transcriptome profiling, luciferase reporter for Pepck promoter, hepatic glucose production assay |
Molecular and cellular biology |
High |
20385766
|
| 2010 |
JARID1B/KDM5B is a corepressor of TIEG1/KLF10: the repression domains of TIEG1 bind the C-terminus of JARID1B. JARID1B overexpression augments TIEG1-mediated repression of Smad7; JARID1B knockdown increases Smad7 mRNA, indicating TIEG1 represses transcription through histone H3K4 demethylation. |
Co-immunoprecipitation (TIEG1–JARID1B), domain mapping, Smad7 reporter assay with JARID1B overexpression/knockdown |
Biochemical and biophysical research communications |
Medium |
20863814
|
| 2011 |
IL-6 activates Tyk2, which phosphorylates TIEG1/KLF10 at Tyr179, promoting non-canonical K27-linked polyubiquitination that inhibits TIEG1 nuclear translocation and thereby abrogates TGF-β-induced Treg development. |
Phosphorylation assays, ubiquitination assays, nuclear fractionation, functional Treg development assay, TRAMP-C2 tumor model in TIEG1-/- mice |
Journal of immunology |
High |
21471442
|
| 2011 |
TIEG1/KLF10 directly binds to and activates the Runx2 promoter (via its zinc finger domain) and physically associates with Runx2 protein to co-activate Runx2 transcriptional activity; TGF-β1 and BMP2 induction of Runx2 requires TIEG1 expression. |
Transient transfection with promoter deletion constructs, chromatin immunoprecipitation, co-immunoprecipitation, adenoviral Runx2 rescue in KO osteoblasts |
PloS one |
High |
21559363
|
| 2011 |
TIEG1/KLF10 suppresses breast cancer cell invasion and mammary tumorigenesis by directly binding to the EGFR promoter at Sp1 sites, recruiting HDAC1, suppressing histone acetylation, and thereby inhibiting EGFR transcription. |
TIEG1 overexpression/knockdown, chromatin immunoprecipitation, co-immunoprecipitation of TIEG1-HDAC1 complex, EGFR promoter binding, invasion assay, xenograft model |
Molecular and cellular biology |
High |
22025675
|
| 2011 |
Klf10 directly modulates transcription of BI-1 (Bax inhibitor-1) by binding to the BI-1 promoter, as confirmed by ChIP-chip, EMSA, and BI-1 promoter mutation that abolishes Klf10-mediated repression; reduced BI-1 increases cytosolic Ca2+ and induces apoptosis in estrogen-responding breast cancer cells. |
ChIP-chip, EMSA, BI-1 promoter luciferase with binding site mutation, si-KLF10 rescue, intracellular Ca2+ measurement |
The international journal of biochemistry & cell biology |
High |
21262377
|
| 2012 |
KLF10 dose-dependently activates p21WAF1/CIP1 transcription independently of p53 and Sp1 binding sites, and KLF10-deficient mice exhibit increased susceptibility to skin tumorigenesis after DMBA/TPA treatment. |
KLF10 KO mouse tumorigenesis model, p21 promoter luciferase assay with deletion/mutation, colony formation assay after H-Ras transfection |
Biochemical and biophysical research communications |
Medium |
22349513
|
| 2013 |
KLF10 stability is regulated by RAF-1-mediated phosphorylation at Thr93 and subsequent interaction with the prolyl isomerase PIN1 (identified by yeast two-hybrid); PIN1 binding (phosphorylation-dependent, via the pThr93-Pro motif) promotes KLF10 protein degradation. |
In vitro and in vivo phosphorylation assays, yeast two-hybrid screening, site-directed mutagenesis of Thr93, protein-protein interaction assays, cycloheximide chase, in vitro kinase assay with RAF-1 |
Biochimica et biophysica acta |
High |
23994618
|
| 2013 |
KLF10 represses FGFR1 promoter activity in myoblasts by binding to the proximal Sp1 binding site of the FGFR1 promoter, competing with Sp1, thereby reducing myoblast proliferation by 86%. |
Southwestern blot, electromobility shift assay (EMSA), chromatin immunoprecipitation, FGFR1 promoter luciferase in myoblasts and Drosophila SL2 cells, cell proliferation assay |
The Journal of biological chemistry |
High |
23569208
|
| 2014 |
KLF10 directly binds to the TGF-βRII promoter in CD8+ T cells, activating its transcription; KLF10-deficient CD8+ T cells show reduced TGF-βRII surface expression and attenuated Smad2 phosphorylation after TGF-β1 stimulation. |
Chromatin immunoprecipitation, TGF-βRII promoter binding assay, KLF10-/- mouse CD8+ T cell phenotyping, flow cytometry for TGF-βRII, phospho-Smad2 measurement, in vivo viral infection model |
American journal of physiology. Cell physiology |
High |
25472963
|
| 2014 |
KLF10 integrates antagonistic epigenetic signals at the FOXP3 promoter: an NH2-terminal Sin3-interacting repressor domain limits KLF10 activation, while inactivation of this domain enables KLF10 to physically associate with the histone acetyltransferase PCAF to induce FOXP3 gene transcription. |
Chromatin immunoprecipitation, genome-integrated reporter assay, functional domain KLF10 mutant proteins, Co-IP with PCAF and Sin3-HDAC complex, primary murine lymphocyte validation |
American journal of physiology. Regulatory, integrative and comparative physiology |
High |
24944246
|
| 2015 |
KLF10 directly binds to the TGF-βRII promoter in macrophages, enhancing its transcription through histone H3 acetylation; KLF10-deficient macrophages show reduced TGF-βRII expression, attenuated Smad2 phosphorylation, and a pro-inflammatory cytokine profile (increased TNF-α, decreased IL-10). |
Chromatin immunoprecipitation, KLF10-/- mouse bone marrow-derived macrophage studies, H3 acetylation assay at TGF-βRII promoter, cytokine ELISA, adoptive transfer of KO macrophages |
American journal of physiology. Gastrointestinal and liver physiology |
High |
26472224
|
| 2015 |
KLF10 transcriptionally activates the SEI-1 promoter and induces SEI-1 protein expression in pancreatic carcinoma cells, subsequently increasing p21Cip1 expression; KLF10-deficient mice show decreased pancreatic islet mass with nuclear accumulation of p21Cip1. |
ChIP-chip identification of SEI-1 as KLF10 target, luciferase promoter assay, KLF10 KO mouse islet histology |
The international journal of biochemistry & cell biology |
Medium |
25578559
|
| 2016 |
TIEG1/KLF10 directly binds to and activates the Osterix promoter (via its zinc finger DNA-binding domain) in osteoblasts; TIEG1 is required for induction of Osterix by TGF-β1 and BMP2. |
Transient transfection with Osterix promoter constructs, chromatin immunoprecipitation, shRNA and CRISPR knockdown of TIEG1, KO osteoblast complementation |
Biochemical and biophysical research communications |
High |
26801561
|
| 2017 |
KLF10 suppresses TGF-β-induced EMT by occupying GC-rich sequences in the SLUG/SNAI2 promoter, recruiting HDAC1, and removing activating histone acetylation marks to repress SLUG transcription. |
KLF10 depletion (siRNA/shRNA), chromatin immunoprecipitation at SLUG promoter, histone acetylation assay, EMT marker panel, lung adenocarcinoma clinical specimens |
Cancer research |
High |
28249899
|
| 2017 |
TIEG1/KLF10 directly represses Smad7 promoter activity by binding a GC-box/Sp1 site at nucleotides -1392 to -1382, thereby promoting Smad2 phosphorylation and enhancing TGF-β/Smad signaling in keloid fibroblasts. |
siRNA knockdown and overexpression, luciferase reporter assay of Smad7 promoter, chromatin immunoprecipitation, collagen production and migration assays |
The Journal of investigative dermatology |
High |
28108300
|
| 2017 |
TIEG1/KLF10 is involved in canonical Wnt signaling in bone: TIEG1 modulates AKT and GSK-3β activity to promote β-catenin nuclear localization, and TIEG1 physically interacts with and serves as a transcriptional co-activator for Lef1 and β-catenin. |
Co-immunoprecipitation (TIEG1–β-catenin, TIEG1–Lef1), subcellular fractionation, AKT/GSK-3β phosphorylation assays, KO mouse bone phenotype analysis |
Nucleic acids research |
High |
28201653
|
| 2017 |
KLF10 directly activates PGC-1α (Ppargc1a) gene transcription by binding to its promoter region, increasing expression of gluconeogenic genes and hepatic glucose output; hepatic KLF10 knockdown in diabetic/obese mice decreases blood glucose. |
Luciferase reporter gene assay, chromatin immunoprecipitation, adenoviral KLF10 overexpression/shRNA in primary hepatocytes and mouse liver, glucose tolerance and pyruvate tolerance tests |
Diabetologia |
High |
28836014
|
| 2017 |
Loss of KLF10 in pancreatic cancer cooperating with KrasG12D increases distant metastases and cancer stemness through activation of SDF-1/CXCR4 and AP-1 pathways; inhibition of the SDF-1/CXCR4 pathway suppresses PDAC progression in KLF10-null context. |
Pdx-1Cre KrasG12D KLF10 conditional KO mouse models, SDF-1/CXCR4 pathway analysis, CXCR4 inhibitor treatment |
Oncogene |
Medium |
28581520
|
| 2018 |
KDM6A (a histone lysine demethylase) upregulates KLF10 in diabetic podocytes, and KLF10 in turn represses nephrin expression by directly binding the nephrin gene promoter and recruiting DNA methyltransferase Dnmt1; KLF10 overexpression also increases KDM6A, forming a positive feedback loop. |
KDM6A/KLF10 overexpression/KO in podocytes, chromatin immunoprecipitation at nephrin promoter, Dnmt1 co-recruitment assay, KDM6A/KLF10 KO mouse diabetic nephropathy model |
EMBO molecular medicine |
High |
30948420
|
| 2018 |
C/EBPβ binds to the KLF10 promoter and transactivates KLF10 expression during mitotic clonal expansion in 3T3-L1 preadipocytes; KLF10 in turn represses C/EBPα promoter activity by recruiting HDAC1, decreasing acetylated histone H4, thereby delaying adipogenesis. |
Chromatin immunoprecipitation, promoter luciferase with deletion/mutation analysis, co-immunoprecipitation (KLF10–HDAC1), siRNA knockdown, histone acetylation assay |
The Journal of biological chemistry |
High |
30026232
|
| 2010 |
HPV-16 E7 directly binds the C-terminus of TIEG1/KLF10 (identified by yeast two-hybrid) and promotes TIEG1 degradation via the ubiquitin pathway, attenuating TIEG1-mediated apoptosis. |
Yeast two-hybrid, co-immunoprecipitation, ubiquitination assay, apoptosis functional assay |
The international journal of biochemistry & cell biology |
Medium |
20691807
|
| 2020 |
CD4+-T-cell-specific KLF10 knockout mice develop obesity, insulin resistance, and fatty liver due to defects in Treg mobilization to liver/adipose tissue and decreased TGF-β3 release; mechanistically, KLF10 KO Tregs exhibit reduced mitochondrial respiration, glycolysis, and PI3K-Akt-mTOR signaling, impairing chemotaxis. Adoptive transfer of WT Tregs fully rescues the phenotype. |
CD4+-T-cell-specific KLF10 KO mice, metabolic phenotyping, Treg adoptive transfer rescue, in vitro TGF-β3 ELISA, metabolic flux analysis (mitochondrial respiration and glycolysis), PI3K-Akt-mTOR signaling assays |
Cell reports |
High |
33378664
|
| 2021 |
KLF10 promotes NASH progression by transcriptionally activating zDHHC7, which palmitoylates CD36 to promote its plasma membrane localization and hepatic lipid accumulation; both zDHHC7 expression and CD36 palmitoylation are required for KLF10's pathogenic role. |
Hepatocyte-specific KLF10 overexpression/depletion in NASH mouse models, transcriptomic analysis, luciferase reporter and ChIP for zDHHC7 promoter, CD36 palmitoylation assay, plasma membrane fractionation |
EMBO reports |
High |
35492028
|
| 2021 |
AMPK phosphorylates KLF10 at Thr189, stabilizing the protein; phosphorylated KLF10 binds the SREBP-1C promoter and represses its transcription, thereby reducing lipogenesis. Hepatic-specific KLF10 KO mice develop more severe NAFLD on a high-fat diet. |
In vitro and in vivo phosphorylation assays, ChIP-chip for target gene identification, SREBP-1C promoter luciferase, hepatocyte-specific KLF10 KO mouse NAFLD model, Western blotting |
Frontiers in molecular biosciences |
High |
34869587
|
| 2021 |
KLF10 binds to the IL-9 promoter and interacts with HDAC1 to inhibit IL-9 transcription in CD4+ T cells; CD4+-T-cell-specific KLF10 deficiency leads to increased IL-9, which drives fibroblast activation, calcium mobilization, and perivascular fibrosis; anti-IL9 antibodies reverse the fibrosis. |
Chromatin immunoprecipitation (KLF10 at IL-9 promoter, HDAC1 interaction), TKO mouse Ang II infusion model, aortic single-cell RNA-seq, cytokine analysis, anti-IL9 therapeutic rescue |
Circulation research |
High |
35440172
|
| 2024 |
Exercise induces KLF10 expression in liver via the cAMP/PKA/CREB pathway; KLF10 promotes fumarate hydratase 1 (Fh1) expression, thereby reducing fumarate accumulation, decreasing H3K4me3 on lipogenic gene promoters, and attenuating lipogenesis to protect against NASH. |
Hepatocyte-specific KLF10 KO and overexpression mouse models, treadmill exercise, cAMP/PKA/CREB pathway inhibitors, fumarate metabolomics, H3K4me3 ChIP at lipogenic gene promoters |
Metabolism: clinical and experimental |
High |
38615945
|
| 2015 |
Computer-aided drug design identified small molecule inhibitors that bind a druggable pocket in the second zinc finger of KLF10, inhibiting KLF10-DNA binding and transcriptional activity, as well as conversion of CD4+CD25- T cells to CD4+CD25+ Tregs. |
CADD virtual screening, KLF10-DNA binding inhibition assays, T regulatory cell conversion assay, KLF10 target gene expression |
Journal of medicinal chemistry |
Medium |
25581017
|
| 2022 |
KLF10 directly binds the ACSM3 promoter and transcriptionally activates it (validated by ChIP and dual-luciferase assay); KLF10-mediated ACSM3 upregulation inhibits PI3K/Akt signaling to suppress melanoma cell proliferation, invasion, and migration. |
ChIP assay, dual-luciferase reporter, KLF10 overexpression and ACSM3 knockdown rescue experiments, PI3K/Akt phosphorylation assays |
Oncology letters |
Medium |
35497935
|
| 2019 |
KLF10 directly regulates the Indian hedgehog (Ihh) promoter activity in mesenchymal stem cells; KLF10 knockdown mimics miR-892b overexpression in enhancing chondrogenesis and inhibiting hypertrophy in TGF-β-mediated chondrogenesis. |
Luciferase assay for Ihh promoter, KLF10 knockdown in hMSC chondrogenesis, miR-892b mimic overexpression, hypertrophic and chondrogenic marker gene analysis |
Molecular therapy. Nucleic acids |
Medium |
31284128
|
| 2012 |
TIEG1/KLF10 missense mutations found in human HCM patients significantly increase PTTG1 promoter activity in transfection/luciferase assays compared to WT TIEG1, and PTTG1 protein is elevated in TIEG1-mutation-positive HCM cardiac tissue by immunohistochemistry. |
Site-directed mutagenesis, transient transfection luciferase assay for PTTG1 promoter, immunohistochemistry of cardiac tissue |
Journal of cellular biochemistry |
Medium |
22234868
|
| 2015 |
TIEG1/KLF10 inhibits Ang II-induced cardiomyocyte hypertrophy by inhibiting the expression and transcriptional activity of GATA4; TIEG1 knockdown upregulates ANF and BNP, while TIEG1 overexpression inhibits hypertrophic gene expression. |
siRNA knockdown and overexpression in cardiomyocytes, cellular surface area measurement, ANF/BNP mRNA quantification, GATA4 transcriptional activity assay |
Journal of cardiovascular pharmacology |
Medium |
26252173
|
| 2017 |
TIEG1/KLF10 directly suppresses SOST (sclerostin) promoter activity; TIEG1 KO osteocytes (shRNA or CRISPR-Cas9) show increased SOST expression and delayed mineralization. Estrogen and ovariectomy modulate SOST expression in a TIEG1-dependent manner in vivo. |
Promoter deletion assay, chromatin immunoprecipitation, shRNA and CRISPR-Cas9 knockdown in IDG-SW3 osteocytes, OVX/ERT studies with mRNA sequencing |
Journal of cellular physiology |
High |
29044507
|
| 2012 |
TIEG1/KLF10 represses stathmin promoter activity in a dose-dependent manner and is required for TGF-β1-induced growth inhibition in hepatocellular carcinoma cells; siRNA knockdown of TIEG1 decreases TGF-β1 sensitivity in Hep3B cells. |
siRNA knockdown, TIEG1 lentiviral overexpression, luciferase assay for stathmin promoter, MTT cell viability assay, DAPI apoptosis staining |
World journal of gastroenterology |
Medium |
22563190
|
| 2016 |
KLF10 acts as a transcriptional repressor of NPRA and directly binds the NPRA promoter; KLF10-deficient mice show increased NPRA expression and exacerbated pulmonary inflammation upon LPS or ovalbumin challenge. |
KLF10 KO mouse pulmonary inflammation model, luciferase reporter assay showing KLF10 repression of NPRA promoter, ChIP confirming KLF10 binding to NPRA promoter, histology |
The international journal of biochemistry & cell biology |
Medium |
27592451
|
| 2022 |
KLF10 directly binds the promoter of LINC00629 (confirmed by ChIP) and activates its transcription; apigenin induces KLF10 which then drives LINC00629 expression to decrease Mcl1 stability and promote apoptosis in oral squamous cell carcinoma. |
Chromatin immunoprecipitation of KLF10 at LINC00629 promoter, luciferase reporter assay, LINC00629-Mcl1 protein interaction and degradation assays |
Aging |
Medium |
36445338
|
| 2020 |
KLF10 deletion in liver leads to increased phosphorylation and nuclear localization of Smad3 under high-sucrose feeding, contributing to liver fibrosis; KLF10 depletion sensitizes primary hepatocytes to TNF-α-induced apoptosis via increased caspase-3 activation. |
Klf10 KO mouse high-sucrose diet model, Smad3 phosphorylation and nuclear localization Western blot/immunofluorescence, primary hepatocyte apoptosis with TNF-α treatment, caspase-3 assay |
International journal of molecular sciences |
Medium |
33396939
|