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
- Electronic nicotine delivery systems (ENDS) may contain or generate low levels of tobacco-specific nitrosamines (TSNAs), including N-nitrosoanatabine (NAT) and N-nitrosoanabasine (NAB), under certain thermal conditions. Given the uncertain long-term carcinogenic effects of ENDS, this study explored potential molecular associations between TSNA-related exposure signatures and LCNEC using an integrative computational framework. - Source: PubMed
Publication date: 2026/09/08
Xiong ZheYin LiuzheYu JiahuiLiu ZhichengWu WeiYang Gang - Atopic dermatitis (AD) is increasingly recognized as a systemic inflammatory disease associated with increased cardiovascular risk, yet the mechanisms linking AD to atherosclerosis and clinically relevant biomarkers of early vascular involvement remain poorly defined. We characterized the circulating proteomic profile of moderate-to-severe AD and identified biomarkers associated with subclinical atherosclerosis. In this cross-sectional study, serum samples from patients with AD (n=34), psoriasis (n=34), and healthy controls (n=20) were analyzed using proteomic panels targeting inflammatory and cardiovascular pathways. Participants underwent carotid and femoral ultrasound to detect atheromatous plaques. Compared with controls, AD showed increased circulating Th2 (CCL13, ST2, IL-13), innate (IL-6, IL-18), Th1 (IFN-γ), and Th17 (IL-17RA) markers, together with cardiovascular-related proteins including CCL19, FGF21, HGF, and P-selectin, with enrichment of atherosclerosis-related pathways. In AD, plaques were associated with higher LDL receptor, CDH5, transferrin receptor, CCL19, and CCL25, and lower IGFBP-2 levels, which also correlated with atherosclerosis burden. A composite proteomic score showed good discrimination of plaques (AUC 0.94) and outperformed traditional cardiovascular risk factors. Proteomic profiles and plaque-associated proteins differed markedly from psoriasis. These findings identify a disease-specific systemic proteomic signature in AD linked to early atherosclerosis and highlight circulating biomarkers with potential relevance for cardiovascular risk stratification. - Source: PubMed
Publication date: 2026/09/09
Berna-Rico EmilioNeria FernandoGómez-de la Fuente EnriquePérez-García BibianaAranda Carlos JAbbad-Jaime de Aragón CarlotaPerez-Bootello JavierDomínguez-López RaquelMonge DianaDavo-Mogica MariaBlauvelt AndrewGonzález-Cantero Álvaro - Astrocytes are essential glial cells that maintain brain homeostasis. Upon brain injury, they become reactive astrocytes with altered morphology, gene expression, and function, including dysregulated Ca signaling implicated in disease development and progression. P2Y1 receptor (P2Y1R), one of Gq-GPCRs, is upregulated in reactive astrocytes across multiple brain disorders, including Alzheimer's disease, epilepsy, and stroke; however, how this upregulation contributes to pathology has remained unclear. To address this question, we generated astrocyte-specific P2Y1R-overexpressing transgenic mice. P2Y1R overexpression in astrocytes induced neuronal hyperexcitability, as evidenced by increased hippocampal neuronal firing, abnormal EEG spikes, and heightened susceptibility to pilocarpine-induced seizures. Dual-color Ca imaging of neurons and astrocytes, electrophysiology, transcriptome analysis of astrocytes, immunohistochemistry, and CRISPR/Cas9-mediated astrocyte-specific knockdown revealed that P2Y1R overexpression amplified both neuron-to-neuron and neuron-to-astrocyte signaling, with astrocytes becoming hypersensitive to neuronal activity-derived ATP. Astrocyte-specific transcriptomic analysis identified insulin-like growth factor binding protein 2 (IGFBP2) as a key downstream effector. IGFBP2, a secreted protein selectively expressed in astrocytes, enhanced glutamatergic synaptic transmission. Furthermore, co-upregulation of P2Y1R and IGFBP2 was confirmed in reactive astrocytes in both kainate-induced epilepsy and middle cerebral artery occlusion stroke models. These findings identify the P2Y1R-IGFBP2 signaling axis as a common pathological feature of reactive astrocytes across brain diseases and establish IGFBP2 as a novel glial-derived factor that could promote neuronal hyperexcitability. - Source: PubMed
Shigetomi EijiKoizumi Schuichi - Adults with Down syndrome (DS) have an increased risk of developing early Alzheimer disease. While our previous cross-sectional study investigated the blood proteome in the context of Alzheimer in DS, identifying CBLN4, CD14, C-X-C motif chemokine 17 (CXCL17), ectodysplasin A2 receptor (EDA2R), glial fibrillary acidic protein (GFAP), insulin-like growth factor binding protein-2 (IGFBP2), neurofilament light (NFL), SEPTIN3, and SPON1 as proteins of interest, longitudinal trajectories remain mostly unexplored. We aimed to characterize the longitudinal dynamics of these plasma proteins to evaluate their potential contribution to disease pathophysiology and associated cognitive decline. - Source: PubMed
Publication date: 2026/09/01
Wagemann OliviaNuebling Georg SSandkühler KatjaWlasich ElisabethLoosli Sandra VPrix CatharinaStockbauer Anna ChristinaMarth LenaForte AnabelVöglein JonathanKatzdobler SabrinaBernhardt Alexander MaximilianMartinez-Murcia Francisco JJiménez-Mesa CarmenHöglinger Günter ULevin Johannes - : The growth hormone (GH)-insulin-like growth factor (IGF) axis is profoundly dysregulated in critical illness. GDF-15 and individual IGF-binding proteins (IGFBPs) have separately been proposed as prognostic biomarkers, but to our knowledge, no prior study has simultaneously characterized all major GH-IGF axis components and GDF-15 in the same critically ill cohort, precluding assessment of their joint intercorrelation structure. : To provide the first simultaneous characterization of the intercorrelation structure among ten GH-IGF axis components and GDF-15 in a single ICU cohort, testing whether this structure is robust to adjustment for illness severity; and, secondarily, to describe admission discriminatory performance relative to APACHE II and SOFA. : This was a prospective observational pilot study of 43 critically ill adults with admission (T01) measurement of ten GH-IGF axis biomarkers and longitudinal follow-up to day 15. Spearman correlations and hierarchical clustering characterized the admission intercorrelation structure; partial correlations adjusting for APACHE II and SOFA, and bootstrap confidence intervals, assessed robustness. Secondary analyses included the examination of admission discrimination (ROC/AUC), a leave-one-out cross-validated combined model, and longitudinal trajectories. All analyses were exploratory, hypothesis-generating, and unadjusted for multiple comparisons unless stated. : Hierarchical clustering identified a coherent cluster comprising GDF-15, IGFBP-1, IGFBP-2, and growth hormone-binding protein (GHBP), distinct from classical GH-resistance markers (GHR vs. healthy controls, GHR vs. admission) and from GH, IGF-1, acid-labile subunit (ALS), and IGFBP-3. Within this cluster, GDF-15 correlated with IGFBP-1 (ρ = 0.65, 95% bootstrap CI 0.44-0.78), IGFBP-2 (ρ = 0.50, CI 0.19-0.71), and GHBP (ρ = 0.47, CI 0.20-0.68); GDF-15 showed no correlation with classical GH-resistance markers. These correlations were essentially unchanged after adjusting for APACHE II or SOFA (partial ρ within 0.03-0.16 of unadjusted values), indicating the structure is not attributable to shared confounding by illness severity. This robustness extended to further adjustment for IL-6, age, BMI, and mechanical-ventilation duration, and results from all 45 pairwise T01 correlations were re-examined with Benjamini-Hochberg false-discovery-rate correction (9 of 11 nominally significant pairs retained q < 0.05). However, the GDF-15-GHBP correlation, unlike the GDF-15-IGFBP-1/IGFBP-2 correlations, attenuated substantially after adjustment for IL-6 and was not consistent across a brain-injury/non-brain-injury subgroup sensitivity analysis, indicating this specific link is less specific than the others. In secondary exploratory analyses, GDF-15 had the highest individual admission AUC (0.74) among biomarkers but was substantially outperformed by APACHE II (AUC 0.90) and SOFA (AUC 0.81); a combined GDF-15 + IGFBP-2 model did not improve on GDF-15 alone. : This study identifies a severity-independent intercorrelation structure linking GDF-15 to inhibitory IGFBPs, distinct from classical GH-resistance signaling, in critically ill patients. Although the findings do not support any clinical application at this stage, further study in adequately powered, multicenter cohorts can be contemplated. - Source: PubMed
Publication date: 2026/07/27
Ilias IoannisKeskinidou ChrysiPoupouzas GeorgiosIssaris VasileiosLotsios Nikolaos SBotoula EfthymiaTzanela MarinellaVassiliadi Dimitra AKokkoris SteliosVrettou Charikleia SVassiliou Alice GDimopoulou Ioanna