Ask about this productRelated genes to: IGFBP2 antibody
- Gene:
- IGFBP2 NIH gene
- Name:
- insulin like growth factor binding protein 2
- Previous symbol:
- IBP2
- Synonyms:
- -
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-09
- Date modifiied:
- 2015-11-12
Related products to: IGFBP2 antibody
Related articles to: IGFBP2 antibody
- Inflammatory bowel disease (IBD) is a systemic disorder that affects not only the gastrointestinal tract but also extraintestinal organs and is associated with a significantly increased risk of osteoporosis. This study aims to investigate the association between plasma proteomic profiles and the subsequent risk of osteoporosis in patients with IBD. - Source: PubMed
Publication date: 2026/08/04
Yue MinYe XiaohuaJin ZhenheYe KexinXu ChengweiZhou TianyuShen Zhe - Although insulin-like growth factor binding protein 2 (IGFBP2) is significantly upregulated in diabetic gastroparesis (DGP) and may regulate ICC mitophagy through its interaction with VDAC1, the precise mechanism of action remains unclear. This study aims to investigate the role and mechanism of IGFBP2 in the pathogenesis of DGP, with a specific focus on its impact on mitochondrial quality control in interstitial cells of Cajal (ICCs). - Source: PubMed
Publication date: 2026/07/27
Yuan XiaoChen YutingQin ZhengranZhang Hong - Insulin-like growth factor binding protein 2 (IGFBP2) has emerged as a multifarious and context-dependent oncoprotein that links several mechanisms in the tumor microenvironment (TME) including oncogenic signaling, extracellular matrix (ECM) remodeling, immune evasion, and therapy resistance. Beyond its established role in modulating IGF signaling, IGFBP2 exerts IGF-independent effects via its RGD integrin-binding motif and nuclear localization signal (NLS). By binding integrins (αvβ3, α5β1), IGFBP2 activates focal adhesion kinase (FAK), which then triggers PI3K/AKT signaling and MAPK/ERK signaling pathways, resulting in enhanced proliferation, migration, invasion, and angiogenesis. Nuclear translocation of IGFBP2, mediated by its NLS, enables direct regulation of gene expression, notably by upregulating epithelial-mesenchymal transition (EMT) transcription factors such as ZEB1, SNAI1, and TWIST1, and regulating immune checkpoint molecules. These actions reshape the TME by increasing angiogenesis, stromal stiffness, and tumor invasiveness. IGFBP2 further sustains survival signals under receptor tyrosine kinase inhibition, enhances tumor cell metabolic adaptation to hypoxia, and supports cancer stemness, all of which drive resistance to chemotherapy, radiotherapy, and immunotherapy. Overexpression of IGFBP2 in cancer is linked to increased tumor aggressiveness, unfavorable prognosis, and general resistance to therapy. Importantly, IGFBP2 functions are highly context-dependent, in some epithelial settings, IGFBP2 sequesters IGFs and dampens IGF-IR signaling, resulting suppression of downstream oncogenic pathways. This duality underscores IGFBP2's nuance and tumor-specific biology. Therapeutic strategies under development specifically target IGFBP2-integrin-mediated signaling and IGFBP2 nuclear activity. There are encouraging results in preclinical studies involving antisense oligonucleotides, monoclonal antibodies, and peptide inhibitors. As both a mediator of oncogenic adaptation and a clinical biomarker, IGFBP2 represents a vulnerability in the TME that may be targeted to improve, personalize, and combine cancer therapies. - Source: PubMed
Publication date: 2026/08/03
Das ProvasConley Shannon MarthaPanja PrasantaBhattacharya ReshamMukherjee Priyabrata - Idiopathic pulmonary fibrosis (IPF) is characterized by failed alveolar epithelial repair and progressive fibrotic remodeling. Although aberrant reprogramming of alveolar type 2 (AT2) cells and accumulation of transitional AT2 states are increasing recognized as central features of IPF, the epithelial-intrinsic mechanisms that initiate these pathogenic states remain incompletely understood. Here, we identify mitochondrial transcription factor A (TFAM), a regulator of mitochondrial DNA maintenance, as a critical regulator of AT2 cell homeostasis. TFAM expression was reduced in AT2 cells from human IPF lungs. Inducible AT2 cell-specific deletion in mice caused spontaneous fibrotic remodeling and increased susceptibility to bleomycin-induced lung injury. TFAM-deficient AT2 cells acquired KRT8 transitional and p21 senescence-associated features before the onset of fibrotic transformation, accompanied by impaired oxidative phosphorylation, redox imbalance, mitochondrial superoxide accumulation, repression of mtDNA-encoded respiratory genes, and disrupted mitochondrial ultrastructure. TFAM-deficient AT2 cells developed a profibrotic secretory program that promoted extracellular matrix deposition and fibroblast activation. We further identified insulin-like growth factor-binding protein 2 (IGFBP2) as a secreted mediator induced in TFAM-deficient AT2 cells. IGFBP2 was elevated in AT2 cells in human IPF lung tissue and bronchoalveolar lavage fluid (BALF) from patients with IPF. IGFBP2 was detected in supernatants from fibrotic human precision-cut lung slices (hPCLS). IGFBP2 neutralization attenuated profibrotic remodeling in fibrotic hPCLS. Collectively, our findings identify TFAM-dependent mitochondrial homeostasis as an epithelial checkpoint linking AT2 cell-state stability to impaired epithelial-mesenchymal crosstalk driving pulmonary fibrosis. - Source: PubMed
Publication date: 2026/07/18
Hu QianjiangOnwuka UgochiCardenes NayraPackwood MadelineHuang Eileen LShi JianMelo-Narvaez Maria CamilaDutta PujaZhou ZiheBeaulieu DelphineChuan ByronSuresh PavanRedding Kevin MichaelTwardowski Laura-MarieVarley ScarlettPineda Ricardo HSembrat JohnSullivan Mara Lisa GroveFranks JonathanWatkins Simon CSt Croix ClaudetteKliment Corrine REickelberg OliverLehmann MareikeBueno MartaKaufman Brett AKönigshoff Melanie - Lipedema is a chronic disorder that predominantly affects women and is characterized by abnormal subcutaneous adipose tissue accumulation, pain, and vascular dysfunction. However, reliable circulating biomarkers that reflect disease-specific pathophysiology are still lacking. This study investigated serum markers associated with adipose tissue, inflammation, and angiogenesis to further elucidate the pathophysiology of lipedema. - Source: PubMed
Publication date: 2026/07/12
Kempa SallyWeiss Thomas STews Hauke ChristianPrantl LukasMüller MartinaBuechler Christa