| 1997 |
LKLF/KLF2 is required to program the quiescent state of single-positive T cells and maintain their viability; LKLF-deficient T cells produced by gene targeting had a spontaneously activated phenotype and died from Fas ligand-induced apoptosis in peripheral lymphoid organs. |
Gene targeting (knockout mouse), in vivo phenotypic analysis of T cell activation and apoptosis |
Science |
High |
9302292
|
| 1997 |
LKLF/KLF2 expressed in vascular endothelial cells is required for tunica media formation and vessel wall stabilization; LKLF-deficient embryos die from hemorrhage with defects in smooth muscle cell organization, reduced pericytes, and decreased extracellular matrix deposition in vessel walls. |
Homologous recombination (knockout mouse), in situ hybridization, immunohistochemistry, electron microscopy |
Genes & development |
High |
9367982
|
| 1998 |
Loss of LKLF/KLF2 causes embryonic lethality with abdominal bleeding, craniofacial abnormalities, and failure of fetal liver erythroid colony formation in vitro, establishing an essential and non-redundant role in embryonic erythropoiesis that cannot be compensated by the closely related EKLF. |
Gene targeting (knockout mouse), in vitro fetal liver erythroid colony assay |
Transgenic research |
High |
9859212
|
| 2001 |
Forced expression of LKLF/KLF2 in Jurkat T cells is sufficient to program a quiescent phenotype (decreased proliferation, reduced cell size, decreased activation markers) partly by decreasing c-Myc expression; the effects of LKLF are mimicked by dominant-negative MadMyc and rescued by c-Myc overexpression. |
Retroviral/plasmid overexpression in Jurkat cells, dominant-negative rescue, gene targeting KO for complementation |
Nature immunology |
High |
11477405
|
| 2002 |
KLF2 directly inhibits PPARγ2 promoter activity (70% inhibition) by binding a specific site in the PPARγ2 promoter, thereby acting as a negative regulator of adipogenesis by repressing PPARγ as well as downstream factors C/EBPα and SREBP1c; KLF2 had no effect on upstream C/EBPβ or C/EBPδ. |
Transient transfection reporter assay, promoter mutational analysis, gel mobility shift assay (EMSA), overexpression in preadipocytes and primary cells |
The Journal of biological chemistry |
High |
12426306
|
| 2003 |
TRAF2 regulates LKLF/KLF2 expression through the p38 MAP kinase pathway (not via TNF signaling or NF-κB); ectopic LKLF expression in TRAF2-deficient cells protected against TNF-induced apoptosis, placing LKLF downstream of TRAF2/p38 in an anti-apoptotic pathway. |
Microarray gene expression comparison of TRAF2−/− vs. WT cells, ectopic expression rescue, pathway inhibitor analysis |
Molecular and cellular biology |
Medium |
12897154
|
| 2004 |
KLF2 inhibits proliferation of Jurkat T leukemia cells by upregulating p21WAF1/CIP1 expression; the functional responsive element in the p21 promoter is the Sp1-3 binding site (not the CACCC site), and both activation and inhibitory domains of KLF2 are required for this effect. |
Tetracycline-inducible expression system, 3H-thymidine uptake assay, luciferase reporter assay, promoter deletion/mutation analysis |
Oncogene |
High |
15361832
|
| 2005 |
KLF2 regulates endothelial thrombotic function by transcriptionally inducing thrombomodulin and eNOS, reducing PAI-1, and inhibiting cytokine-induced tissue factor expression; siRNA knockdown of KLF2 reduces antithrombotic gene expression and reduces blood clotting time in functional clotting assays. |
Adenoviral overexpression, siRNA knockdown, gene expression analysis, in vitro clotting assays |
Circulation research |
High |
15718498
|
| 2005 |
KLF2 (LKLF) is regulated by shear stress in vivo at high-shear arterial sites and acts as a transcriptional regulator of vascular tone genes; KLF2 repression by siRNA suppressed the flow response of endothelin-1, adrenomedullin, and eNOS, establishing KLF2 as a downstream mediator of the shear stress-to-gene expression axis. |
Carotid artery collar model (in vivo), siRNA knockdown, in situ hybridization, laser microdissection/RT-PCR, shear stress chamber experiments |
The American journal of pathology |
High |
16049344
|
| 2007 |
KLF2 inhibits proinflammatory gene expression in endothelial cells under laminar shear stress by suppressing nuclear binding activity of ATF2; siRNA knockdown of ATF2 suppressed basal proinflammatory gene expression under no-flow conditions, placing KLF2-mediated ATF2 inhibition as the mechanism of atheroprotection. |
Genome-wide expression profiling, promoter analysis, ATF2 nuclear binding activity assay, siRNA knockdown, HUVEC shear stress experiments |
Blood |
Medium |
17244683
|
| 2010 |
B cell-specific KLF2 deficiency leads to decreased expression of trafficking molecules CD62L and β7-integrin, a drastic reduction in the B1 B-cell pool, increased transitional and marginal zone B-cell numbers, increased apoptosis, and impaired proliferation after BCR cross-linking; S1PR1 expression was unexpectedly minimally altered in B cells. |
B cell-specific conditional KO mouse, flow cytometry, gene expression analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
21187410
|
| 2011 |
KLF1 and KLF2 directly bind the promoters of human ε- and γ-globin genes, mouse Ey- and βh1-globin genes, and the β-globin locus control region in embryonic blood cells, positively regulating embryonic and fetal β-globin gene expression; KLF1 loss reduces H3K9Ac and H3K4me3 marks at these loci. |
Chromatin immunoprecipitation (ChIP) with embryonic blood cells, conditional KO mouse models, dual transgenic human β-globin locus mouse model |
The Journal of biological chemistry |
High |
21610079
|
| 2014 |
KLF2 represses PFKFB3 promoter activity, thereby inhibiting endothelial glycolysis under laminar shear stress; KLF2 overexpression reduces glucose uptake, glycolytic enzyme expression (PFKFB3, PFK-1, HK2), and angiogenic sprouting, effects partially reversed by PFKFB3 overexpression. |
Seahorse flux analysis, glucose uptake assays, RNA sequencing, luciferase reporter assay, siRNA/overexpression, endothelial-specific KLF2 KO mouse |
Arteriosclerosis, thrombosis, and vascular biology |
High |
25359860
|
| 2014 |
In zebrafish, loss of CCM proteins upregulates klf2 mRNA through a β1 integrin-dependent mechanism (independent of blood flow), which causes enhanced egfl7 expression and angiogenic signaling; downregulation of β1 integrin rescues CCM cardiovascular malformations, establishing a β1 integrin-Klf2-Egfl7 pathway regulated by CCM proteins. |
Zebrafish CCM morpholino/mutant model, HUVEC siRNA knockdown, in vivo rescue experiments |
Developmental cell |
Medium |
25625207
|
| 2014 |
KLF2 mutations in splenic marginal zone lymphoma (predominantly in the C-terminal zinc finger domains) inactivate the ability of KLF2 to suppress NF-κB activation by TLR, BCR, BAFFR, and TNFR signaling, as shown by functional assays. |
Whole exome sequencing, functional NF-κB reporter assays with mutant KLF2 constructs |
Leukemia |
Medium |
25428260
|
| 2015 |
KLF2 restrains CD4+ T follicular helper (Tfh) cell differentiation through two mechanisms: (1) promoting S1PR1 expression to control T cell localization (S1PR1 downregulation is required for Tfh generation), and (2) inducing Blimp-1 expression which represses Bcl-6, thereby impairing Tfh differentiation; KLF2 also induces T-bet and GATA3 to enhance Th1 differentiation. |
Inducible KLF2 deletion in activated CD4+ T cells, KLF2 overexpression, gene expression analysis, in vivo Tfh quantification |
Immunity |
High |
25692701
|
| 2016 |
CCM disease pathogenesis involves gain of MEKK3-KLF2/4 signaling: loss of CCM complex (KRIT1, CCM2, PDCD10) increases MEKK3 kinase activity which elevates KLF2 and KLF4 expression and Rho activity in endothelial cells of CCM lesions; endothelial-specific loss of Mekk3, Klf2, or Klf4 prevents lesion formation and rescues lethality in a neonatal mouse CCM model. |
Neonatal mouse CCM model, endothelial-specific conditional KO of Mekk3/Klf2/Klf4, human CCM lesion immunostaining, CCM2 disease-causing mutation analysis (abrogates MEKK3 interaction) |
Nature |
High |
27027284
|
| 2016 |
KDM3A histone demethylase maintains KLF2 expression through H3K9 demethylation at the KLF2 locus; KLF2 directly activates IRF4 transcription, and IRF4 reciprocally upregulates KLF2, forming a positive autoregulatory circuit; KLF2 silencing triggers apoptosis in multiple myeloma cells and decreases ITGB7-dependent cell adhesion to bone marrow stromal cells. |
siRNA knockdown (KDM3A, KLF2, IRF4), ChIP for H3K9 methylation, in vitro and in vivo MM models, gene expression analysis |
Nature communications |
High |
26728187
|
| 2016 |
KLF2 is a transcription factor required for homeostatic NK cell proliferation and survival; KLF2 deficiency promotes spontaneous proliferation of immature NK cells and regulates a subset of homing receptors that allow mature NK cells to access IL-15-rich microenvironments; KLF2-deficient NK cells undergo apoptosis due to IL-15 starvation. |
Gene-targeted KO mouse models, ex vivo NK cell proliferation assays, homing receptor expression analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
27114551
|
| 2017 |
Inducible endothelial-specific deletion of both Klf2 and Klf4 (EC-DKO) causes acute death from myocardial infarction, heart failure, and stroke with profound compromise of vascular integrity and dysregulation of the coagulation system; a single allele of either gene is sufficient for survival, establishing that KLF2 and KLF4 together control a large segment of the endothelial transcriptome essential for vascular integrity. |
Inducible endothelial-specific double KO mouse (Klf2/Klf4), transcriptome analysis, coagulation assays |
JCI insight |
High |
28239661
|
| 2017 |
KLF2 inhibits endothelial cell migration by KLF2-dependent transcriptional repression of PAK1 (a pro-migratory Rac/Cdc42 mediator); Erk5 activation (via constitutively active MEK5, statins, or shear stress) decreases PAK1 mRNA and protein through KLF2 but not KLF4; PAK1 re-expression or KLF2 knockdown restores migration in Erk5-activated ECs. |
Constitutively active MEK5 expression, siRNA knockdown (KLF2, KLF4), PAK1 re-expression rescue, migration assays, statin/shear stress treatment |
Cardiovascular research |
Medium |
25388666
|
| 2014 |
IKKβ inhibition increases thrombomodulin (TM) expression and function through a KLF2-dependent mechanism: IKKβ inhibition causes KLF2 overexpression and enhanced KLF2 binding to the TM promoter (demonstrated by ChIP); KLF2 knockdown completely attenuates IKKβ-inhibition-mediated TM upregulation. |
IKKβ chemical inhibitors, siRNA/shRNA knockdown, ChIP assay, luciferase reporter assay, flow cytometry, APC generation assay |
Journal of thrombosis and haemostasis |
High |
25039491
|
| 2015 |
KLF2 directly binds the AQP1 (aquaporin-1) promoter (demonstrated by ChIP) and positively regulates AQP1 expression in endothelial cells; inflammatory stimuli repress AQP1 in an effect restrained by KLF2 overexpression. |
Chromatin immunoprecipitation (ChIP), KLF2 overexpression, siRNA, gene expression profiling, immunohistochemistry in human vascular tissue |
PloS one |
Medium |
26717516
|
| 2015 |
miR-302-367 downregulates Erk1/2, which increases KLF2 expression, which in turn upregulates S1PR1 and VE-cadherin, suppressing angiogenesis and improving vascular stability; this Erk1/2-Klf2-S1pr1 pathway was validated by genetic S1pr1 deletion which reversed the antiangiogenic effects of miR-302-367. |
Endothelial-specific miR302-367 overexpression in mice, S1pr1 genetic deletion, retinal angiogenesis assay, tumor angiogenesis models |
Circulation research |
Medium |
27756792
|
| 2015 |
Simvastatin activates KLF2 expression through a Rac1-Rab7-autophagy dependent mechanism; KLF2 induction in turn promotes further activation of autophagy, forming a positive feedback loop; this autophagy-KLF2 relationship modulates endothelial phenotype and survival in acute liver injury. |
Pharmacological inhibition (GGTI-298, statins, resveratrol), adenoviral KLF2 overexpression, autophagic flux assays, LSEC and HUVEC models, pre-clinical liver I/R models |
Journal of hepatology |
Medium |
27545498
|
| 2018 |
KLF2 directly regulates osteoblast differentiation by binding to and physically interacting with Runx2, promoting Runx2 expression and activity; KLF2 overexpression increases Alp, Osx, Ocn and mineralization while knockdown has opposite effects. |
Overexpression and siRNA knockdown in MC3T3-E1 cells and primary osteoblasts, co-immunoprecipitation (KLF2-Runx2 interaction) |
Laboratory investigation |
Medium |
30429507
|
| 2019 |
KLF2 regulates osteoclastogenesis by modulating Beclin1 (BECN1)-mediated autophagy; KLF2 knockdown increases H3K9 and H4K8 acetylation in the Becn1 promoter region (demonstrated by ChIP), increasing Becn1 expression; KLF2 overexpression reduces these histone acetylation marks and decreases autophagy and osteoclast differentiation. |
ChIP assay for histone modifications at Becn1 promoter, adenoviral KLF2 overexpression, siRNA knockdown, 3-methyladenine autophagy inhibition, arthritis mouse model |
Autophagy |
Medium |
30894058
|
| 2015 |
PIEZO1 mechanosensitive channel mediates shear stress-induced KLF2/4 expression through a CaMKII-MEKK3-ERK5 signaling axis: shear stress activates PIEZO1, causing calcium influx that activates CaMKII, which interacts with and activates MEKK3, promoting MEKK3/MEK5/ERK5 signaling to induce KLF2/4 transcription; endothelial-specific Piezo1 deletion reduces KLF2/4 expression in vivo. |
Endothelial-specific Piezo1 knockout mice, PIEZO1 receptor antagonist, siRNA, CaMKII interaction/activation assays, shear stress experiments |
Cells |
Medium |
35883633
|
| 2015 |
P2X4 purinergic receptor mediates shear stress-induced KLF2 expression in endothelial cells; shear-induced ATP release activates P2X4, promoting ERK5 phosphorylation and KLF2 upregulation; a loss-of-function P2X4 variant (Tyr315>Cys) blocks ATP-induced KLF2 expression. |
siRNA knockdown of P2X4, pharmacological P2X4 antagonist, transient transfection of mutant P2X4, HUVEC shear stress experiments |
Purinergic signalling |
Medium |
25563726
|
| 2017 |
Endothelial KLF2 mediates protection against cardiac maladaptive remodeling via a Klf2-Foxp1-TGFβ1 pathway; endothelial-specific KLF2 inhibition reverses simvastatin-mediated reduction of fibroblast proliferation and myofibroblast formation; KLF2 directly regulates TGFβ1 and Foxp1 in endothelial cells, and loss of Foxp1 phenocopies KLF2 inhibition. |
Endothelial-specific siRNA delivery via RGD-magnetic nanoparticles in vivo, pressure overload model, gene expression analysis, in vitro EC studies |
Theranostics |
Medium |
33408770
|
| 2020 |
KLF2 directly promotes Vav1 transcription in adult DRG neurons; increased Vav1 then promotes axon regeneration by activating Rac1 GTPase; Klf2 is induced by retrograde Ca2+ signaling from injured axons, establishing a Klf2-Vav1-Rac1 axis in peripheral nerve regeneration. |
RNA-seq after sciatic nerve crush, ChIP for KLF2 at Vav1 promoter, siRNA/overexpression knockdown in DRG neurons, Vav1 KO functional rescue |
Experimental neurology |
Medium |
34147481
|
| 2021 |
KLF2 inhibits ferroptosis in clear cell renal cell carcinoma by transcriptionally repressing GPX4; KLF2 deficiency impairs GPX4 repression, promoting migration and invasion; reverting KLF2 expression in vivo decreases pulmonary metastases, and GPX4 overexpression reverses KLF2-mediated anti-metastatic effects. |
KLF2 overexpression/knockdown in vitro and in vivo, GPX4 expression analysis, ferroptosis assays, xenograft mouse model |
Cancer letters |
Medium |
34520818
|
| 2020 |
KLF2 directly binds the IRF4 promoter (demonstrated by dual luciferase reporter gene assay and ChIP) and upregulates IRF4 expression; IRF4 in turn binds the HDAC7 promoter to increase HDAC7 expression, forming a KLF2-IRF4-HDAC7 neuroprotective pathway in hypoxic-ischemic brain damage. |
Dual luciferase reporter gene assay, ChIP, adenoviral KLF2 overexpression, in vivo HIBD rat model, OGD neuron model |
Cell death discovery |
Medium |
35091544
|
| 2019 |
IRF2BP2 regulates KLF2 expression; KLF2 overexpression in osteoclast precursors inhibits osteoclast differentiation by downregulating c-Fos, NFATc1, and TRAP, while KLF2 overexpression in osteoblasts enhances differentiation by upregulating Runx2, ALP, and BSP; IRF2BP2 effects on bone cells are reversed by KLF2 downregulation. |
Overexpression and siRNA knockdown in osteoclast precursor and osteoblast cell lines, differentiation marker assays, epistasis by KLF2 siRNA rescue |
BMB reports |
Medium |
31186082
|
| 2017 |
Restoring KLF2 expression in the carotid body of heart failure rabbits (via adenoviral transfection) reduces sympathetic nerve activity, arrhythmia incidence, and chemoreflex sensitivity; lentiviral KLF2 siRNA in the carotid body increases chemoreflex sensitivity and sympathetic activation, establishing KLF2 as a regulator of carotid body chemoreflex function. |
In vivo adenoviral KLF2 transfection and lentiviral siRNA knockdown in carotid body, measurement of ventilation, renal SNA, ECG, arrhythmia, breathing patterns |
The Journal of physiology |
Medium |
29023738
|
| 2022 |
KLF2 regulates neutrophil NETosis pathway activated by chronic angiotensin II infusion; mechanistically, KLF2 controls neutrophil activation partly through crosstalk with HIF1 signaling; KLF2-dependent NETosis triggers sporadic thrombosis in small myocardial vessels leading to cardiac hypertrophy. |
Mouse model of Ang II-induced cardiac dysfunction, neutrophil-specific KLF2 manipulation, NET/thrombosis targeting, HIF1 signaling analysis |
The Journal of clinical investigation |
Medium |
34793333
|
| 2020 |
KLF2 regulates chemoreflex-related carotid body function by modulating BDNF/TrkB pathway in microglial cells under oxygen-glucose deprivation; KLF2 overexpression increases BDNF and TrkB levels and protects against OGD-induced apoptosis; these KLF2 effects are blocked by BDNF/TrkB inhibitor K252a, establishing KLF2 upstream of BDNF/TrkB signaling. |
Adenoviral KLF2 overexpression in BV2 cells, OGD model, K252a (BDNF/TrkB inhibitor) epistasis, cell viability/apoptosis assays |
Gene |
Low |
31821872
|
| 2021 |
KLF2 inhibits TGF-β/Smad signaling in hepatocellular carcinoma cells by inhibiting the transcriptional activity of Smad2/3 and Smad4, creating a negative feedback loop; stably expressed KLF2 attenuates TGF-β-induced MMP2 upregulation and cancer cell motility. |
Luciferase reporter assay for Smad transcriptional activity, stable KLF2 expression, wound-healing and transwell assays, MMP2 expression analysis |
Acta biochimica et biophysica Sinica |
Medium |
32318691
|
| 2020 |
KLF2 induces KLF2-mediated autophagy in dental pulp-derived stem cells (DPSCs) during osteoblast differentiation; ChIP analysis confirmed KLF2 and active epigenetic marks (H3K27Ac and H3K4me3) are upregulated in the ATG7 promoter region during OB differentiation; a metabolic shift from mitochondrial respiration to glycolysis occurs during OB differentiation. |
ChIP for KLF2 and histone marks at ATG7 promoter, Seahorse flux analysis, ROS measurements, gain/loss-of-function of KLF2 and autophagy genes (ATG7, BECN1) |
Redox biology |
Medium |
32777717
|
| 2024 |
METTL3-mediated N6-methyladenosine (m6A) modification of KLF2 mRNA plays a crucial role in protecting pulmonary artery endothelial cells from EndMT; m6A modification stabilizes KLF2 mRNA; mutations in m6A sites of KLF2 mRNA compromise KLF2 expression and its protective effect; KLF2 modulates SM22 expression through direct binding to its promoter. |
RNA methylation quantification, m6A-RIP-qPCR, mRNA stability assay, m6A site mutation, dual-luciferase assay for KLF2 binding to SM22 promoter, endothelial-specific Mettl3 KO mice |
Cellular & molecular biology letters |
Medium |
38741032
|
| 2017 |
Simvastatin upregulates S1PR1 transcription via KLF2: simvastatin induces KLF2 recruitment to the S1PR1 promoter (demonstrated by ChIP); KLF2 silencing significantly attenuates simvastatin-induced S1PR1 promoter activity and augmented S1PR1 agonist-mediated barrier enhancement. |
ChIP for KLF2 at S1PR1 promoter, luciferase reporter assay, siRNA KLF2 knockdown, transendothelial electrical resistance assay, in vivo mouse lung microarray |
Pulmonary circulation |
Medium |
28680571
|
| 2025 |
KLF2 is required to suppress the exhaustion-promoting transcription factor TOX and to enable TBET to drive effector differentiation during acute LCMV infection; KLF2 KO results in aberrant differentiation to exhausted-like CD8 T cells during acute infection, and KLF2 is necessary to maintain a polyfunctional tumor-specific progenitor state. |
In vivo CRISPR-Cas9-based perturbation sequencing (~40 TFs), KLF2 KO during LCMV infection, TOX and TBET expression analysis |
Science |
High |
39946463
|
| 2023 |
In CAR T cells, KLF2 acts as a hub transcription factor in the effector gene network and enhances effector CD8+ T cell differentiation while preventing terminal exhaustion; FOXP1 (hub in stem-like network) and KLF2 (hub in effector network) reciprocally regulate checkpoints of stem-like to effector transition. |
Single-cell paired chromatin accessibility and transcriptome profiling (ATAC+RNA-seq) in CAR T cells, enhancer network analysis, FOXP1/KLF2 functional perturbations |
Nature immunology |
Medium |
38012417
|
| 2019 |
KLF2 directly regulates osteoclastogenesis and osteoblast differentiation; IRF2BP2 overexpression suppresses osteoclast differentiation and enhances osteoblast differentiation through KLF2; effects are reversed by downregulating KLF2, establishing IRF2BP2-KLF2 as a regulatory axis in bone homeostasis. |
Overexpression and siRNA knockdown of IRF2BP2 and KLF2 in bone cells, epistasis rescue, differentiation marker assays |
BMB reports |
Medium |
31186082
|
| 2019 |
KLF2 interacts with FOXO4 and cooperates with FOXO4 to induce p21 expression and cellular senescence in pancreatic cancer cells; downregulation of either p21 or FOXO4 impairs KLF2-induced senescence. |
Co-immunoprecipitation (KLF2-FOXO4 interaction), KLF2 overexpression/knockdown, p21 and FOXO4 siRNA knockdown, senescence assays |
Experimental cell research |
Medium |
31866399
|
| 2021 |
KLF2 interacts with hexokinase 1 (HK1) and inhibits HK1-mediated glucose metabolism reprogramming, thereby suppressing endothelial-to-mesenchymal transition (EndMT); KLF2 mediates the suppressive effect of BDNF on diabetic intimal calcification through this KLF2/HK1 axis. |
Co-immunoprecipitation (KLF2-HK1 interaction), HK1 knockdown, KLF2 overexpression/knockdown, glycolysis measurements in HUVECs |
Cellular signalling |
Medium |
33253911 34363795
|
| 2015 |
KLF2 interacts with β-catenin and negatively regulates β-catenin/TCF signaling in pancreatic ductal adenocarcinoma cells, thereby inhibiting cell growth and migration. |
Co-immunoprecipitation (KLF2-β-catenin), overexpression in PDAC cells, TCF reporter assay, migration/growth assays |
Tumour biology |
Low |
26449825
|
| 2021 |
In zebrafish, klf2a and klf2b are required for Notch signaling activation in the endocardium and heart regeneration; klf2 gene expression is regulated by primary cilia-dependent mechanosensing of blood flow changes, placing klf2 downstream of primary cilia in a cilia-klf2-Notch axis. |
Zebrafish heart regeneration model, klf2a/klf2b morpholino knockdown, primary cilia mutants, Notch reporter assays |
Protein & cell |
Medium |
32249387
|
| 2021 |
In zebrafish valvulogenesis, Erk5-Klf2-Wnt9a signaling (activated by shear stress) drives Wnt9a production, which induces ingression of endocardial cells into cardiac jelly to form abluminal cell populations; this mechanosensitive Klf2 pathway runs in parallel with Notch-Dll4 lateral inhibition to sculpt valve leaflets. |
Zebrafish valvulogenesis model, klf2 and wnt9a genetic/morpholino manipulations, Notch-Dll4 pathway epistasis, live imaging |
Cell reports |
Medium |
34610316
|