| 2010 |
DIP2A was identified as a receptor for FSTL1 on endothelial cells. Co-immunoprecipitation demonstrated direct physical interaction between FSTL1 and DIP2A. Knockdown of DIP2A by siRNA reduced FSTL1 binding to cells, diminished FSTL1-stimulated endothelial cell survival, migration, and tube formation, and inhibited FSTL1-induced Akt phosphorylation. In cardiac myocytes, DIP2A ablation reduced FSTL1-mediated protection against hypoxia/reoxygenation-induced apoptosis and suppressed FSTL1-induced Akt phosphorylation. |
Co-immunoprecipitation, siRNA knockdown, cell survival/migration/differentiation assays, Western blot for Akt phosphorylation |
The Journal of biological chemistry |
High |
20054002
|
| 2011 |
Fstl1 directly interacts with BMP4 and negatively regulates BMP4/Smad1/5/8 signaling during lung development. Fstl1-deficient mice showed elevated pSmad1/5/8 activity, impaired alveolar epithelial differentiation, and insufficient surfactant production. Reducing BMP signaling with Noggin rescued pulmonary atelectasis in Fstl1-deficient mice, placing Fstl1 as a BMP4 antagonist in lung morphogenesis. |
Genetic knockout mouse model, direct binding assay (Fstl1-BMP4 interaction), Smad1/5/8 phosphorylation assays, Noggin rescue epistasis experiment, in vitro BMP4-induced surfactant gene expression assay |
Proceedings of the National Academy of Sciences of the United States of America |
High |
21482757
|
| 2012 |
Fstl1 antagonizes BMP signaling in the developing ureter. Fstl1-null mice showed elevated pSmad1/5/8 in ureters. In vitro, Fstl1 was shown to directly bind to ALK6, a BMP receptor specifically expressed in ureteric epithelial cells, providing a mechanism for Fstl1-mediated BMP pathway suppression during ureter development. |
Genetic knockout mouse model, in vitro binding assay (Fstl1-ALK6 interaction), pSmad1/5/8 immunostaining |
PloS one |
Medium |
22485132
|
| 2013 |
The miR-198/FSTL1 switch is controlled post-transcriptionally: TGF-β signaling downregulates KSRP (KHSRP), which is required for miR-198 processing from the FSTL1 primary transcript. When KSRP is inhibited, the transcript is redirected toward FSTL1 protein translation. FSTL1 protein expression promotes keratinocyte migration, while miR-198 inhibits migration by targeting DIAPH1, PLAU, and LAMC2. |
Human ex vivo organ culture wound model, TGF-β signaling manipulation, KSRP binding/knockdown experiments, luciferase reporter assays, keratinocyte migration assays |
Nature |
High |
23395958
|
| 2015 |
Epicardial FSTL1 protein promotes cardiomyocyte cell cycle entry and division. Epicardial FSTL1 declines after myocardial infarction and is replaced by myocardial expression. Myocardial FSTL1 does not promote regeneration. Application of human FSTL1 protein via an epicardial patch stimulates cardiomyocyte proliferation and improves cardiac function in mouse and swine MI models. |
Epicardial patch delivery of recombinant human FSTL1 protein, cardiomyocyte cell cycle entry and division assays, mouse and swine MI models, transgenic FSTL1 overexpression |
Nature |
High |
26375005
|
| 2006 |
MyoD directly activates expression of miR-206, which targets sequences in the Fstl1 3'UTR and is sufficient to suppress Fstl1 expression during skeletal muscle differentiation. |
Fibroblast-to-myoblast conversion by MyoD overexpression, luciferase reporter assays with Fstl1 3'UTR, miR-206 gain-of-function experiments |
The Journal of cell biology |
High |
17030984
|
| 2017 |
TGF-β1 upregulates Fstl1 expression in lung fibroblasts via the Smad3-c-Jun pathway. While TGF-β1 activates Smad, MAPK, and Akt pathways, only Smad2/3 inhibition eliminated TGF-β1-induced Fstl1 expression. A functional c-Jun transcription site in the Fstl1 promoter was identified by luciferase reporter analysis. |
Mouse pulmonary fibroblast cultures, pharmacological pathway inhibitors, luciferase reporter assays with Fstl1 promoter constructs, qRT-PCR and Western blot |
American journal of physiology. Lung cellular and molecular physiology |
Medium |
28495857
|
| 2018 |
Fstl1 promotes temozolomide resistance in glioblastoma by competitively binding DIP2A and blocking DIP2A nuclear translocation. DIP2A normally cooperates with the HDAC2-DMAP1 complex to enhance H3K9Ac deacetylation and prevent MGMT transcription, increasing temozolomide sensitivity. FSTL1 binding to DIP2A prevents this, leading to increased promoter H3K9Ac and MGMT expression. DIP2A depletion abolished the effects of Fstl1 on MGMT expression and temozolomide resistance. |
Co-immunoprecipitation (Fstl1-DIP2A interaction), siRNA knockdown, chromatin immunoprecipitation (H3K9Ac), gene expression assays, in vivo xenograft models |
Oncogene |
High |
30542120
|
| 2019 |
Crystal structure of the FK domain of murine Fstl1 was solved at high resolution, revealing that the FK domain forms a stable dimer in both solution and crystal. The FK domain was found to be indispensable for proper Fstl1 function during TGF-β signaling transduction. The potential for Fstl1 to function as a dimer during interaction with TGF-β (which itself forms dimers) was proposed based on structural data. |
X-ray crystallography of FK domain, solution studies (dimerization), functional assays of FK domain mutants in TGF-β signaling |
Protein science : a publication of the Protein Society |
High |
31351024
|
| 2022 |
Macrophage FSTL1 promotes liver fibrosis by binding directly to PKM2 via its FK domain, promoting PKM2 phosphorylation and nuclear translocation, reducing PKM2 ubiquitination, enhancing PKM2-dependent glycolysis, and increasing M1 macrophage polarization via NF-κB pathway activation. Myeloid-specific FSTL1 knockout attenuated liver fibrosis and reduced M1 polarization. |
Myeloid-specific FSTL1 knockout mice, Co-IP (FSTL1-PKM2 direct binding via FK domain), Western blot for PKM2 phosphorylation and nuclear translocation, ubiquitination assays, glycolysis measurements, in vitro macrophage polarization assays, pharmacological PKM2 activator (DASA-58) |
Gut |
High |
35140065
|
| 2022 |
FSTL1 interacts with Wnt ligands (specifically Wnt3a) and Frizzled receptors (specifically FZD4) but not with the co-receptor LRP6. FSTL1 interacts with Wnt3a through its extracellular calcium-binding (EC) domain and VWC domain, and with FZD4 through its EC domain. FSTL1 increased the association of Wnt3a with FZD4 and thereby enhanced Wnt/β-catenin signaling and fibrogenesis in obstructed kidneys. |
Co-immunoprecipitation (FSTL1-Wnt3a, FSTL1-FZD4 interactions), domain deletion analysis, FSTL1 overexpression/inhibition in obstructed mouse kidneys, Wnt/β-catenin reporter assays, single-cell RNA-Seq for expression localization |
The Journal of biological chemistry |
High |
35525270
|
| 2021 |
FSTL1 secreted by activated fibroblasts binds to TLR4 on hepatocellular carcinoma cells, resulting in activation of AKT/mTOR/4EBP1 signaling, promoting HCC growth, metastasis, and maintenance of tumor-initiating cells. |
Recombinant FSTL1 treatment of HCC cells and 3D organoids, receptor binding assay (TLR4 identified as receptor), Western blot for AKT/mTOR/4EBP1 signaling, conditioned medium experiments, preclinical mouse models with FSTL1 blockade |
Cancer research |
Medium |
34551961
|
| 2020 |
Dynamic resistance exercise stimulates skeletal muscle FSTL1 secretion. FSTL1 binds receptor DIP2A on endothelial cells and activates Smad2/3 signaling to promote cardiac angiogenesis. TGFβR1 inhibitor reduced pSmad2/3 and VEGF-A expression but did not affect FSTL1-DIP2A direct Smad2/3 activation, demonstrating that the FSTL1-DIP2A-Smad2/3 axis is independent of TGFβR1. |
Rat MI model with resistance exercise, AAV-FSTL1 injection, recombinant FSTL1 treatment of HUVECs, TGFβR1 inhibitor pharmacological epistasis, Western blot for DIP2A and pSmad2/3, immunofluorescence, tubule assay |
Journal of sport and health science |
Medium |
33246164
|
| 2018 |
FSTL1 promotes cardiac angiogenesis and myocardial energy substrate metabolism normalization in heart failure via AMPK activation. FSTL1 stimulated oxygen consumption through AMPK activation in primary cardiac and skeletal muscle myocytes in vitro. |
Conscious dog HF model with acute and chronic FSTL1 infusion, radiolabeled substrate tracking (3H-oleate, 14C-glucose), in vitro primary myocyte assays with AMPK pathway analysis |
Circulation. Heart failure |
Medium |
29317401
|
| 2017 |
In glioblastoma, Fstl1 interacts with BMP4 but not with BMPR2, competitively inhibiting BMP4-BMPR2 association. Fstl1 overexpression suppressed BMP4/Smad1/5/8 signaling pathway activation, promoting glioma cell proliferation, while BMP4 overexpression reversed this effect. |
Co-immunoprecipitation (Fstl1-BMP4 and Fstl1-BMPR2 interactions), Western blot for pSmad1/5/8, cell proliferation and colony formation assays, orthotopic xenograft, BMP4 rescue experiment |
Cellular physiology and biochemistry |
Medium |
29212066
|
| 2017 |
FSTL1 blocks Wnt7a-mediated repression of ERK phosphorylation, enabling MMP9 production that degrades the extracellular matrix and facilitates metastasis. Separately, EGF hijacks the miR-198/FSTL1 switch to sustain FSTL1 translation, driving metastasis through parallel DIAPH1 and FSTL1 pathways. |
Head and neck squamous cell carcinoma cell lines, Wnt7a pathway manipulation, ERK phosphorylation assays, MMP9 expression and activity assays, FSTL1 gain/loss-of-function, migration/invasion assays |
The Journal of experimental medicine |
Medium |
28827448
|
| 2017 |
Macrophage-derived Fstl1 induces oncostatin M (OSM) expression, promoting asthmatic airway remodeling. Macrophage-specific Fstl1 knockout (Lys-Cre/Fstl1Δ/Δ) reduced airway remodeling and OSM levels. Exogenous Fstl1 induced airway remodeling and increased OSM, while anti-OSM antibody blocked Fstl1-induced remodeling, eosinophilic inflammation, and airway hyperresponsiveness. |
Macrophage-specific conditional Fstl1 knockout mice, allergen challenge model, recombinant Fstl1 administration, anti-OSM antibody blockade, airway remodeling and inflammation readouts |
Journal of immunology |
High |
26355153
|
| 2017 |
Knockdown of Fstl1 in hepatic stellate cells suppressed proliferation and reduced α-SMA and collagen I expression in TGF-β1-treated HSCs. Mechanistically, Fstl1 knockdown decreased Smad3 phosphorylation in TGF-β1-induced HSCs, placing Fstl1 as a positive regulator of TGF-β1/Smad3 signaling in liver fibrosis. |
siRNA knockdown of Fstl1 in hepatic stellate cells, Western blot for pSmad3, α-SMA, collagen I, cell proliferation assay |
Molecular medicine reports |
Medium |
28901425
|
| 2017 |
Fstl1 is essential for lung airway and vascular smooth muscle formation. Fstl1 was localized to lung smooth muscle cells. Fstl1 knockout impaired airway smooth muscle differentiation, associated with decreased myocardin/SRF transcription factors. Fstl1 knockout also caused hyperplasia of pulmonary artery vascular smooth muscle. |
Fstl1-lacZ reporter mouse, Fstl1 knockout allele, histological analysis of trachea/bronchi/pulmonary artery, immunostaining for myocardin/SRF |
PloS one |
Medium |
28574994
|
| 2017 |
Fstl1 deletion from the endocardial/endothelial lineage (Tie2-Cre) causes sustained BMP and TGFβ signaling after birth, resulting in ongoing endocardial-to-mesenchymal transition, deformed mitral valves, cardiac hypertrophy, and heart failure. This shows that endocardial FSTL1 normally restrains BMP/TGFβ signaling to maintain valve homeostasis. |
Conditional knockout (Tie2-Cre; Fstl1 flox), echocardiography, electrocardiography, histology, BMP/TGFβ signaling markers |
Arteriosclerosis, thrombosis, and vascular biology |
Medium |
28705792
|
| 2020 |
Endothelial cell-specific FSTL1 knockout led to increased pSMAD3 in vascular mural cells colocalizing with αSMA in vein walls, increased collagen deposition, and cardiac/vascular fibrosis. TGFβ pathway inhibitor treatment reduced the αSMA abnormalities, demonstrating that endothelial FSTL1 normally suppresses TGFβ/SMAD3 signaling in vascular mural cells. |
Conditional endothelial FSTL1 knockout mouse (vs. smooth muscle and hematopoietic cell KOs as controls), pSMAD3 immunostaining, TGFβ inhibitor rescue, collagen deposition assay |
Arteriosclerosis, thrombosis, and vascular biology |
Medium |
32078339
|
| 2023 |
Skeletal muscle IRF4 transcriptionally regulates FSTL1 (dual luciferase assay confirmed IRF4 binding to FSTL1 promoter). FSTL1 mediates inter-organ crosstalk between skeletal muscle and the liver in NASH via different receptors (DIP2A and CD14) on different liver cell types. Restoring FSTL1 in muscle of F4MKO mice was sufficient to restore liver pathology. |
Muscle-specific IRF4 knockout mice, proteomics, dual luciferase reporter assay (IRF4-FSTL1 promoter), co-culture experiments with liver cells, AAV-mediated FSTL1 rescue |
Nature communications |
Medium |
37770480
|
| 2019 |
FSTL1 directly increases expression of MMP-1, MMP-13, iNOS, COX-2, IL-1β, TNF-α, and IL-6 in chondrocytes in a dose-dependent manner, and activates NF-κB and promotes p65 phosphorylation, establishing NF-κB as the signaling pathway mediating FSTL1 pro-inflammatory effects in chondrocytes. |
Recombinant FSTL1 treatment of rat chondrocytes, PCR, ELISA, Western blot for NF-κB pathway components (p65 phosphorylation) |
Journal of cellular and molecular medicine |
Medium |
30644158
|
| 2020 |
FSTL1 promotes nitric oxide-induced chondrocyte apoptosis by activating the SAPK/JNK/Caspase3 signaling pathway. FSTL1 overexpression increased apoptosis in SNP-treated chondrocytes, upregulated MMP1/3/9 and Bax, and reduced Bcl-2 and collagen. The caspase inhibitor Ac-DEVD-FMK impaired FSTL1-induced chondrocyte apoptosis. |
FSTL1 overexpression plasmid transfection in chondrocytes, flow cytometry for apoptosis, Western blot for SAPK/JNK/Caspase3 pathway, caspase inhibitor rescue |
Gene |
Medium |
31927008
|
| 2017 |
FSTL1 knockdown in airway smooth muscle cells inhibited PDGF-BB-induced proliferation, arrested cell cycle at G2/M, and reduced migration. Mechanistically, FSTL1 knockdown downregulated PDGF-BB-induced phosphorylation of ERK and AKT in ASM cells. |
siRNA knockdown of FSTL1 in human ASM cells, cell proliferation assay, cell cycle analysis by flow cytometry, migration assay, Western blot for p-ERK and p-AKT |
Molecular medicine reports |
Medium |
28393245
|
| 2017 |
FSTL1 activates Wnt/β-catenin signaling through integrin β3 in breast cancer cells, promoting stemness and chemoresistance. Luciferase assays demonstrated that miR-137 reduces FSTL1 mRNA and protein levels, identifying FSTL1 as a direct miR-137 target. |
TOP/FOP flash Wnt reporter assay, colony and tumor sphere formation, luciferase assay for miR-137 targeting of FSTL1, Western blot for pathway components |
Cancer biology & therapy |
Medium |
30336071
|
| 2015 |
Fstl1 is expressed in brain by pia mater but not in the ventricular zone; FSTL1 from pia mater is required for radial glial cell morphology. Conditional Fstl1 ablation in both expression domains disrupted RGC basal process organization and caused mislocalization of upper-layer projection neurons. VZ-only Fstl1 deletion did not affect RGC morphology. BMP, AKT/PKB, Cdc42, GSK3β, integrin and reelin signaling were unchanged, indicating a unique mechanism. |
Conditional Fstl1 knockout mice (EIIa-Cre and Emx1-IREScre lines), cortical histology, immunostaining for RGC markers and signaling pathway components |
Molecular brain |
Medium |
26382033
|
| 2025 |
Host FSTL1 enhances rapid recycling of CCR2 to the plasma membrane via activation of the CD14/TLR4/NF-κB/ATP6V1G2 axis, leading to early recruitment of Ly6C+ monocytes/macrophages. This early inflammatory macrophage recruitment is required for MSC-mediated antifibrotic effects in liver cirrhosis. |
Fstl1-deficient mice, recombinant FSTL1 rescue, mechanistic dissection of CD14/TLR4/NF-κB/ATP6V1G2 pathway, CCR2 membrane recycling assays, macrophage depletion/tracking experiments, MSC infusion models |
Signal transduction and targeted therapy |
Medium |
40050288
|
| 2019 |
FSTL1 promotes alveolar epithelial cell senescence by enhancing TGF-β1 signaling, and this enhancement is dependent on SENP1-mediated deSUMOylation. TGF-β1-induced FSTL1 upregulates SENP1 expression in senescent AECs, and interfering with SENP1 inhibited FSTL1-dependent promotion of AEC senescence and improved pulmonary fibrosis. |
TGF-β1 treatment of AECs, SENP1 siRNA knockdown, senescence assays, Western blot for FSTL1 and SENP1, in vivo bleomycin mouse model |
Cell biology international |
Medium |
37369969
|
| 2021 |
FSTL1 activates the NLRP3/IL-1β signaling pathway in macrophages, contributing to asthmatic airway inflammation. Pretreatment with MCC950 (NLRP3 inhibitor) significantly reduced NLRP3 and IL-1β production induced by FSTL1 in mice and in alveolar macrophage MH-S cells. |
Fstl1 heterozygous knockout mice, OVA asthma model, recombinant FSTL1 injection, MCC950 pharmacological inhibitor, siFSTL1, Western blot and ELISA for NLRP3/IL-1β |
Inflammation research |
Medium |
34076707
|
| 2020 |
FSTL-1 attenuation in hypomorphic mice causes spontaneous emphysema independent of smoke. Recombinant FSTL-1 treatment of macrophages attenuated NF-κB p65 phosphorylation in an Nr4a1-dependent manner, identifying a FSTL-1→Nr4a1→NF-κB signaling axis in lung macrophage immune tolerance. |
FSTL-1 hypomorphic mice, lung morphometry and pulmonary function, RNA-seq identifying Nr4a1, in vitro macrophage recombinant FSTL-1 treatment with NF-κB p65 phosphorylation assay, Nr4a1 dependence testing |
American journal of respiratory and critical care medicine |
Medium |
31834999
|
| 2013 |
FSTL1 secreted by Snail-positive tumor cells promotes bone metastasis through two mechanisms: direct mediation of tumor cell invasion and bone tropism, and expansion of CD45−ALCAM+ pluripotent mesenchymal stem-like cells from bone marrow, which both directly induce bone metastasis and generate CD8low T cells with weak CTL activity. RNAi-mediated FSTL1 attenuation prevented bone metastasis and reversed these immune dysfunctions. |
RNAi knockdown of FSTL1 in tumor cells, flow cytometry for ALCAM+ cell expansion and CD8 T cell characterization, in vivo bone metastasis models, in vitro CTL assays |
Cancer research |
Medium |
23966294
|
| 2018 |
FSTL1 interacts with VIM (vimentin) in colorectal cancer cells. This interaction was identified by co-immunoprecipitation and mediates FSTL1's role in activating focal adhesion signaling and cytoskeleton rearrangement to promote CRC metastasis. TGFβ1-Smad2/3 signaling (via Smad3 transcription factor) was identified as an upstream regulator of FSTL1 protein expression. |
Co-immunoprecipitation (FSTL1-VIM), focal adhesion signaling pathway analysis, Smad3 ChIP/reporter for FSTL1 transcriptional regulation, in vitro migration/invasion assays, in vivo liver metastasis model |
Cell death & disease |
Medium |
29844309
|
| 2017 |
Fstl1 promotes glioma stem cell self-renewal through autocrine FSTL1 interacting with TLR2, which inhibits EGFR endocytosis-lysosomal degradation, resulting in activation of the PI3K-AKT signaling pathway. FSTL1 also promotes M2 macrophage polarization via TLR2 signaling. |
FSTL1 knockout in GSC cell lines, TLR2 receptor identification, EGFR endocytosis assays, PI3K-AKT pathway Western blot, mouse GBM models, macrophage polarization assays |
Cancer letters |
Medium |
39722404
|
| 2021 |
FSTL1 promotes myocardial fibrosis via a USP10/Notch1 signaling axis. FSTL1 activation of USP10 (a Notch1 deubiquitinase) stabilizes NICD1 (Notch1 intracellular domain), which suppresses myocardial fibrosis. Pharmacological inhibition of USP10 (spautin-1) or Notch signaling (LY3039478) abolished the protective effects of FSTL1 in diabetic MI mice. |
AAV9-FSTL1 intracardiac delivery in T2DM-MI mice, USP10 inhibitor (spautin-1) and Notch inhibitor (LY3039478) epistasis experiments, cardiac fibrosis markers, Western blot for USP10/Notch1/NICD1 |
Frontiers in cell and developmental biology |
Medium |
34957094
|
| 2023 |
FSTL1 initiates angiogenesis in endothelial cells by opening intercellular junctions via activation of the Src kinase pathway. FSTL1 increased Src phosphorylation and VEGFR2 phosphorylation, decreased VE-Cadherin, Occludin, Connexin-43, and Claudin-5 expression, and increased endothelial permeability. Src inhibitor (but not VEGFR2 inhibitor) blocked FSTL1-induced effects. H2S upregulated FSTL1 in skeletal muscle by increasing HuR levels, which stabilized FSTL1 transcript. |
Recombinant FSTL1 treatment of HUVECs, Src and VEGFR2 pharmacological inhibitors, immunostaining for junction proteins, wound-healing migration assay, permeability assay, HuR siRNA knockdown, mouse hindlimb ischemia model |
American journal of physiology. Cell physiology |
Medium |
37694287
|
| 2019 |
miR-29a in mesenchymal stem cells suppresses FSTL1 expression and secretion (validated by dual luciferase reporter assay). This reduces FSTL1 in conditioned medium, which in turn inhibits the JAK2/STAT3 pathway in cardiac myocytes and promotes myocyte apoptosis after hypoxia-reoxygenation injury. |
Dual luciferase reporter assay (miR-29a targeting FSTL1), miR-29a overexpression in MSCs, FSTL1 measurement by ELISA in conditioned medium, JAK2/STAT3 Western blot in H9c2 cells, flow cytometry for apoptosis |
Cardiovascular pathology |
Medium |
31945680
|
| 2024 |
FSTL1 promotes nucleus pulposus cell senescence via TLR4/NF-κB signaling. Recombinant FSTL1 upregulated p16 and p21, increased SA-β-gal-positive cells, induced SASP, and disrupted ECM balance. TLR4 inhibition partly reversed these effects. FSTL1 siRNA in a rabbit puncture IVDD model reduced disc degeneration. |
Recombinant FSTL1 treatment of NPCs, TLR4 inhibitor rescue, FSTL1 siRNA in vitro and in vivo (rabbit IVDD model), senescence assays (SA-β-gal, p16/p21), Western blot for TLR4/NF-κB |
Inflammation |
Medium |
38316670
|
| 2017 |
BBS4 regulates FSTL1 mRNA levels and also independently modulates FSTL1 secretion. FSTL1 functions as a novel regulator of ciliogenesis, creating a regulatory loop between FSTL1 and cilia. BBS4, cilia, and FSTL1 are coordinated during 3T3-L1 differentiation, with FSTL1 influencing this process at least partly by modulating ciliogenesis. |
BBS4 knockdown/knockout in cells, FSTL1 mRNA quantification, FSTL1 secretion assay, ciliogenesis assays (cilia length/frequency), 3T3-L1 differentiation with FSTL1 manipulation |
Scientific reports |
Medium |
28852127
|
| 2010 |
Fstl1 is a 'preadipokine' that is highly expressed in 3T3-L1 preadipocytes and dramatically downregulated early in differentiation to adipocytes. The Fstl1 protein is secreted by preadipocytes. Negative transcriptional regulation of Fstl1 is mediated by Kruppel-like factor 15 (KLF15), as identified by luciferase reporter assays with Fstl1 5' flanking region constructs. |
Northern blot, Western blot of conditioned media, luciferase reporter assays with Fstl1 5' flanking region constructs, KLF15 expression, multiple adipogenesis model time courses |
Mechanisms of development |
Medium |
20043993
|