ABI3BP
- Known as:
- ABI3BP
- Catalog number:
- 000957A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABI3BP
Related genes to: ABI3BP
- Gene:
- ABI3BP NIH gene
- Name:
- ABI family member 3 binding protein
- Previous symbol:
- -
- Synonyms:
- NESHBP, DKFZP586L2024, TARSH
- Chromosome:
- 3q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-30
- Date modifiied:
- 2015-11-17
Related products to: ABI3BP
Related articles to: ABI3BP
- : Congenital pulmonary airway malformation (CPAM) is a rare developmental disorder characterized by cystic lung lesions, yet its extracellular matrix (ECM) composition remains poorly understood. This study employed decellularization and data-independent acquisition (DIA) proteomics to compare ECM profiles between cystic (CPAM) and histologically normal non-diseased (ND) regions from the lungs of four patients. : The decellularized scaffolds retained their native architecture with minimal residual DNA (<50 ng/mg). Proteomic analysis revealed 431 differentially expressed proteins (DEPs), with 171 upregulated and 260 downregulated in CPAM. Key findings revealed CPAM-specific enrichment of collagens (COL4A6, COL4A2, COL10A1, COL21A1 and PIIINP), glycoproteins (SPP1, FRAS1, FREM1, FREM2, LTBP1 and FBLN7), ECM regulators (TENM2, ROR2 and OMD), and ECM-affiliated proteins (ANXA7), alongside downregulation of glycoproteins (VASN and ABI3BP), proteoglycans (PODN and MXRA7), ECM regulators (SCARA5, PAPPA, SAA4, CPXM1, CTSC, THY1, SERPINA6/A1/D1, BSG, LYVE1, ITIH4 and CD44), and ECM-affiliated proteins (LGALSL). Pathway analysis highlighted the dysregulation of TGF-β, PI3K-AKT, and mTOR signaling in CPAM and aberrant ECM-cell interactions in pathogenesis. We also evaluated their functional properties and investigated the impact of ECM-based hydrogels on recellularization. : These findings provide a comprehensive proteomic atlas of CPAM ECM alterations, offering insights into disease mechanisms and potential therapeutic targets. - Source: PubMed
Publication date: 2026/08/30
Li YananYang PingYuan MiaoZhu XinglongMao ShengqiangYang YingYao MenglinChen FeiZhou YanyanBao JiXu ChangLi Yi - The extracellular matrix (ECM) plays a critical role in tumor progression by modulating cell adhesion, migration, and signaling; however, its contribution to metastatic progression in spontaneous mammary tumors remains poorly understood. Mammary tumors are among the most common neoplasms in female dogs and share histopathological and molecular similarities with human breast cancer, supporting their use as a comparative oncology model. To investigate ECM remodeling during tumor progression, we analyzed normal, non-metastatic, and metastatic canine mammary tissues using histological approaches and label-free quantitative proteomics. Publicly available human breast cancer transcriptomic datasets were interrogated for validation of conserved molecular signatures. Proteomic profiling identified 12 differentially expressed ECM-related proteins: eight were upregulated (COL12A1, COL4A1, COL4A2, SERPINH1, SERPINF1, HTRA1, TNC, PCOLCE) and four were downregulated (MMRN1, ABI3BP, DPT, OGN). The downregulated proteins were further validated in human breast cancer transcriptomes. Collectively, these findings indicate active ECM remodeling during tumor progression, characterized by increased expression of proteins associated with matrix stiffness and invasiveness. This study highlights evolutionarily conserved mechanisms of ECM dysregulation in breast cancer and identifies potential matrix targets for translational research and biomarker development. - Source: PubMed
Publication date: 2026/03/24
de Almeida Bruno SousaRocha Gisele VieiraNunes SimoneZanette Dalila LuciolaBatista MichelEstrela-Lima AlessandraRegis-Silva Carlos GustavoDamasceno Karine Araújo - Podocyte injury is a hallmark of chronic kidney disease (CKD) and organ failure, but whether different injury signals perturb unified or distinct molecular targets remains unclear. Using human induced pluripotent stem cell (hiPSC)-derived podocytes, we modeled cellular injury via exposure to diabetic, inflammatory, chemical toxin, biomechanical, and infectious stressors. Transcriptomic analysis revealed both shared and unique changes in gene expression across injury modes. While drug-induced injuries triggered broader transcriptional responses, conserved pathways related to lysosome function, RNA metabolism, and immune activation were identified across models. Importantly, we discovered NEU1, CD82, ABI3BP, and ADAM17 as targets of human podocyte injury. Analysis of multiple kidney disease patient biopsies confirmed enrichment of these targets, underscoring their in vivo relevance and potential as therapeutic targets. These findings highlight the predictive power of human-relevant experimental models and provide insight into podocyte injury responses, offering a framework for future precision medicine approaches. - Source: PubMed
Publication date: 2026/04/02
Barreto Amanda DJiang BowenBurt Morgan ADimitrakakis NikolaosMusah Samira - Blood-brain barrier (BBB) disruption represents acritical pathological featurein the pathogenesis of stroke. The extracellular matrix plays acritical rolein preserving the structural and functional integrity of the BBB. ABI3BP, an extracellular matrix protein, participatesin stem cell proliferation and differentiation, cellular senescence, tumor suppression, and extracellular matrix remodeling. However, the function and mechanism of ABI3BP in cerebral ischemia-reperfusion injury (IRI) remain unclear. In this study, we found that ABI3BP mRNA increased while protein expression decreased in the ischemic cortex, and serum ABI3BP level rose post-IRI. The thrombin inhibitor dabigatran reverses the reduction of ABI3BP after I/R injury. Thrombin hydrolyzed ABI3BP at arginine 337. Recombinant ABI3BP crossed the BBB, reduced infarct volume, improved neurological scores, restored blood flow, and decreased BBB leakage by upregulating ZO-1/Occludin in ischemic brain tissue. ABI3BP inhibits the expression of cleaved caspase-3 and increases the expression of Bcl-2/Bax, p-Akt/Akt, and p-PI3K/PI3K in vivo and in vitro. IRI induced the hydrolysis and decrease of endogenous ABI3BP level. Supplementation of recombinant ABI3BP protects against cerebral IRI by preserving BBB integrity, enhancing tight junction proteins, and suppressing endothelial apoptosis via PI3K/Akt signaling. Conclusively, these findings suggest that ABI3BP protects BBB integrity, potentially by restoring tight junction protein expression and inhibiting endothelial cell apoptosis after IRI, which suggests its promise as a therapeutic agent in ischemic stroke. - Source: PubMed
Publication date: 2026/03/14
Wang WanChen JieSong Wen-JingYang Yi-CiYin Qi-LongLi Li-LiZhang Meng-NanSu Rui-QiQin Zi-LuWen Zhen-FuQi Su-HuaHuang Lin-Yan - Reliable detection of robust biomarkers from high-dimensional transcriptomic data remains a major challenge in computational oncology. Traditional approaches often suffer from overfitting and poor generalization due to the high dimensionality of genomic data and limited sample sizes. This study aims to identify an optimal, biologically meaningful subset of mRNA biomarkers capable of distinguishing ovarian cancer samples from healthy controls using an integrated machine learning-based feature selection framework. - Source: PubMed
Publication date: 2026/01/28
Thelagathoti Rama KrishnaJiang ChaoChandel Dinesh STom Wesley ASarmiento CleoKrzyzanowski GaryOlou AppolinaireFernando M Rohan