| 2012 |
Heterozygous loss-of-function mutations or deletions in TGFB2 cause aortic root aneurysm in Tgfb2+/- mice with biochemical evidence of increased canonical and noncanonical TGF-β signaling, indicating that TGFB2 haploinsufficiency paradoxically upregulates TGF-β signaling in aortic tissue. |
Genetic mouse model (Tgfb2+/- haploinsufficient mice), western blotting for signaling markers, compound mutant mice with Fbn1(C1039G/+) |
Nature genetics |
High |
22772368 22772371
|
| 2012 |
TGFB2 haploinsufficiency (frameshift and nonsense mutations causing loss of function) predisposes to thoracic aortic aneurysm and dissection; paradoxically, aortic tissue from affected individuals shows increased TGF-β2 expression and immunostaining, suggesting an initial decrease in cellular TGF-β2 leads to a secondary compensatory increase. |
Genome-wide linkage analysis, whole-exome sequencing, Sanger sequencing, immunostaining of aortic tissue from affected individuals |
Nature genetics |
High |
22772371
|
| 2018 |
ΔNp63α transcriptionally represses TGFB2 expression; upon ΔNp63α depletion, TGFB2 is upregulated, which activates RHOA and induces cell cycle arrest in squamous cell carcinomas. Ectopic TGFB2 activates RHOA and impairs SCC proliferation, and TGFB2 neutralization restores cell proliferation during ΔNp63α depletion. |
Genome-wide CRISPR screen, RHOA activity assays, transcriptome analysis, ΔNp63α knockdown, ectopic TGFB2 expression, TGFB2 neutralizing antibody |
Cell reports |
High |
30232004
|
| 2019 |
Constitutive activation of a TGFB2 enhancer, maintained through epigenetic memory (H3K27ac), drives autocrine TGFβ2 signaling and enforces a profibrotic synthetic state in SSc fibroblasts. NF-κB and BRD4 inhibition suppresses TGFB2 enhancer activity and reverses dermal fibrosis in patient skin explants. |
Chromatin accessibility profiling (ATAC-seq), transcriptome profiling, targeted epigenetic editing (CRISPRi), NF-κB and BRD4 inhibition, patient skin explants |
Science translational medicine |
High |
31217334
|
| 2016 |
RUNX1 depletion in hESCs specifically compromises TGFB2 (but not TGFB1) signaling, impairing cell motility and epithelial-to-mesenchymal transition during mesendodermal differentiation. Reintroduction of TGFB2 (not TGFB1) rescues both decreased motility and deregulated epithelial marker expression caused by RUNX1 loss. |
RUNX1 depletion by siRNA, transcriptome profiling, cell motility assays, rescue experiments with exogenous TGFB2 and TGFB1 |
Stem cell reports |
Medium |
27720906
|
| 2021 |
HOXA10 binds to the TGFB2 promoter (shown by ChIP-qPCR), promotes TGFB2 transcription and secretion, thereby triggering TGFβ/Smad signaling with nuclear Smad2/3 accumulation, which in turn upregulates METTL3 expression and promotes EMT in gastric cancer cells. CoIP demonstrated Smad proteins mediate METTL3 expression. |
ChIP-qPCR, dual-luciferase reporter assay, CoIP, western blot, colorimetric m6A assay, in vivo lung metastasis rescue models |
Journal of experimental & clinical cancer research |
Medium |
33563300
|
| 2024 |
METTL14-mediated N6-methyladenosine (m6A) modification post-transcriptionally stabilizes TGFB2 mRNA; TGFB2 then upregulates SREBF1 and downstream lipogenic enzymes via PI3K-AKT signaling to promote lipid accumulation and gemcitabine resistance in pancreatic ductal adenocarcinoma. |
RNA-seq on gemcitabine-resistant PDAC cells, bioinformatic analysis, m6A modification assays, TGFB2 silencing, lipidomic profiling, PI3K/AKT pathway inhibition, PDX mouse model |
Oncogene |
Medium |
38914663
|
| 2024 |
Heterozygous mutations in the straitjacket subdomain of the latency-associated peptide (LAP) of pro-TGF-β2 cause Camurati-Engelmann disease type II by disrupting LAP conformation, reducing TGF-β2 inactivation, and increasing TGF-β2/SMAD signaling activity. iPS-cell-derived osteogenic differentiation from a CED2 patient showed significantly enhanced ossification. |
Exome sequencing, structural simulations of mutant LAPs, TGF-β2/SMAD signaling activity assay, in vitro osteogenic differentiation from CED2 patient-derived iPS cells |
Journal of human genetics |
Medium |
39014191
|
| 2025 |
TGFB2 signals through TGFBR3 (betaglycan) for SMC differentiation in a manner distinct from other TGFβ isoforms. TGFB2 haploinsufficiency (TGFB2KO/+) impairs differentiation of second heart field-derived SMCs, and TGFBR3KO/KO prevents molecular rescue of TGFB2KO/+ by exogenous TGFB2 supplementation, demonstrating TGFBR3 dependence in TGFB2-mediated SMC differentiation. |
hiPSC-derived SMC differentiation, CRISPR/Cas9 gene editing, siRNA experiments, 3D SMC tissue ring constructs, human aortic tissue analysis |
Stem cells translational medicine |
Medium |
40139558
|
| 2025 |
Histone H3K18 lactylation at the TGFB2 promoter (mediated by P300 and GCN5 as candidate transferases) upregulates TGFB2 expression in pressure-overloaded hearts; cardiac-specific Tgfb2 knockdown reversed the prohypertrophic effects, while Tgfb2 overexpression promoted cardiomyocyte hypertrophy via PI3K/AKT/mTOR signaling. |
CUT&TAG, ChIP-qPCR, coimmunoprecipitation (for transferases), nascent RNA-seq, AAV-shRNA knockdown, lentiviral overexpression, pharmacological PI3K/AKT inhibition, mouse transverse aortic constriction model |
Circulation research |
Medium |
41376590
|
| 2023 |
NFATc1 regulates TGFB2 transcription in trabecular meshwork (TM) cells in a cell-cycle-dependent manner: dexamethasone-induced TGFB2 mRNA upregulation occurs in proliferating but not quiescent TM cells, and is inhibited by NFATc1 inhibitors (cyclosporine A or 11R-VIVIT). |
NFATc1 inhibition (cyclosporine A, 11R-VIVIT), cell cycle arrest by contact inhibition or serum starvation, RT-qPCR, Ki-67/p21 cell cycle markers |
Cells |
Medium |
36766846
|
| 2019 |
A ~100 bp enhancer region downstream of TGFB2 (containing variant rs1690789) contacts the TGFB2 promoter in human lung fibroblasts as shown by chromatin conformation capture; CRISPR/Cas9 deletion of this region decreased TGFB2 expression, establishing a regulatory mechanism linking a GWAS variant to TGFB2 expression in fibroblasts. |
GWAS, chromatin conformation capture (3C), CRISPR/Cas9 targeted deletion in primary human lung fibroblasts, eQTL analysis |
eLife |
Medium |
31343404
|
| 2022 |
TGFB2 secreted by oocytes induces cumulus expansion through TGFBR1/TGFBR2-SMAD2/3 signaling in cumulus cells; TGFB2 increased expression of expansion-related genes in oocytectomized complexes in the presence of EGF, and this effect was blocked by TGF-β signaling inhibitor SD208 or by Tgfbr2 depletion in granulosa cells. |
Oocytectomized (OOX) complex culture, exogenous TGFB2 supplementation, SD208 inhibitor treatment, Tgfbr2-specific conditional knockout mice (Zp3-Cre and conditional Cre in granulosa cells), RT-qPCR |
Molecular reproduction and development |
Medium |
36128893
|
| 2010 |
TGF-β2 confers amoeboid-like motility on Theileria-infected leukocytes through a transcription-independent mechanism involving cytoskeletal remodeling via Rho kinase (ROCK) activation; exogenous TGF-β2 rescued invasiveness of attenuated vaccine lines, and TGF-β2 levels correlated with increased actin dynamics in lamellipodia and podosomal structures. |
Exogenous TGF-β2 rescue experiments, fluorescence microscopy, time-lapse video microscopy for actin dynamics, ROCK pathway analysis |
PLoS pathogens |
Medium |
21124992
|
| 2021 |
β-cell miR-21 directly targets and represses Tgfb2 and Smad2 mRNAs (confirmed by pulldown and luciferase assays), leading to reduced β-cell identity markers and glucose-stimulated insulin secretion in both in vitro and in vivo zebrafish and mouse models. |
RT-PCR, immunoblot, pulldown assay, luciferase assay, transgenic zebrafish and mouse models of β-cell-specific pre-miR-21 overexpression |
Molecular metabolism |
Medium |
34246804
|
| 2025 |
SMC-specific Tgfb2 conditional knockout in mice causes rapidly progressive thoracic aortic aneurysms with dissection and rupture. Loss of SMC-derived TGFβ2 suppresses canonical SMAD2/3 phosphorylation, activates non-canonical MAPK (p38 and ERK1/2) signaling, and causes SMC de-differentiation (reduced Acta2, Myh11) with ECM disorganization (elastic fiber fragmentation, increased collagen/proteoglycans). |
Tamoxifen-inducible SMC-specific Cre (Myh11CreERT2), ROSA lineage reporter, histological/morphometric analyses, western blotting for SMAD2/3, p38, ERK1/2, gene expression profiling |
bioRxivpreprint |
Medium |
bio_10.1101_2025.10.01.679917
|
| 1997 |
TGF-β2 secreted by glioma cells decreases TNF-induced VCAM-1 expression on glioma cells and brain-derived endothelial cells; glioma supernatant alone reproduced this effect on CNS endothelial cells in co-culture. |
Co-culture of A-172 glioma cells with CNS endothelial cells, VCAM-1 expression assay, glioma supernatant experiments |
Journal of neuroimmunology |
Low |
9058771
|
| 2025 |
FTO demethylates m6A modifications on TGFB2 mRNA in human BMSCs, increasing TGFB2 expression and promoting osteogenic differentiation; TGFB2 knockdown inhibited osteogenic differentiation downstream of FTO. |
m6A-seq, FTO knockdown by shRNA, TGFB2 knockdown, osteogenic differentiation assays |
Oral diseases |
Low |
40127138
|
| 2025 |
TIPE activates the P38 MAPK signaling pathway in colorectal cancer cells, leading to increased TGFB2 expression and secretion, which then acts on extracellular macrophages to induce M2 polarization, creating a feedback loop enhancing CRC malignant behavior. |
TIPE overexpression/knockdown, western blot for P38 MAPK, TGFB2 ELISA, macrophage polarization assays, animal experiments |
Journal of leukocyte biology |
Low |
40391468
|
| 2025 |
RUNX1 promotes cervical cancer cell proliferation by upregulating TGFB2 expression, which activates the MAPK pathway; TGFB2 inhibition impaired MAPK pathway activation and reversed the proliferative effects of RUNX1 overexpression. |
RUNX1 overexpression/knockdown, TGFB2 inhibition, MAPK pathway western blot, cell cycle and proliferation assays |
Scientific reports |
Low |
39747496
|
| 2025 |
TGFB2 knockdown in H9c2 cells subjected to oxygen-glucose deprivation promoted viability and inhibited apoptosis, reducing cleaved Caspase-3/Caspase-3 and Bax protein levels while increasing Bcl-2, implicating TGFB2 in cardiomyocyte apoptosis signaling in ischemia. |
TGFB2 knockdown, CCK-8 assay, flow cytometry for apoptosis, western blot for caspase-3, Bax, Bcl-2 |
Cardiovascular toxicology |
Low |
40080329
|
| 2023 |
TCF12 directly binds the TGFB2 promoter and activates TGFB2 transcription (established by ChIP and dual-luciferase reporter assay), promoting melanoma cell proliferation and metastasis downstream. |
RNA-seq, qPCR, immunoblotting, ChIP, dual-luciferase reporter assay, subcutaneous tumor formation assay |
Cancers |
Low |
37760480
|
| 2025 |
STAT2 and SMAD3 are upstream transcription factors for TGFB2 in chicken granulosa cells: DNA pull-down and mass spectrometry identified STAT2 binding to the TGFB2 promoter, and SCENIC single-cell network analysis confirmed this regulatory interaction; the JAK/STAT-TGFB2-SMAD3 axis mediates granulosa cell degeneration during follicular atresia. |
DNA pull-down assay, mass spectrometry, SCENIC analysis of single-cell RNA sequencing data, ChIP validation |
Poultry science |
Low |
40902342
|