Ask about this productRelated genes to: PARVB Blocking Peptide
- Gene:
- PARVB NIH gene
- Name:
- parvin beta
- Previous symbol:
- -
- Synonyms:
- CGI-56
- Chromosome:
- 22q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-26
- Date modifiied:
- 2016-10-05
Related products to: PARVB Blocking Peptide
Related articles to: PARVB Blocking Peptide
- UA-2012 (and related non-myristoylated analog UA-1907) is a lead alpha-helical cyclic peptide which inhibits the focal adhesion kinase (FAK)-paxillin protein-protein interaction (PPI) and is being evaluated for the treatment of cutaneous melanoma. However, the development of an empirical approach to measure PPI inhibitor selectivity remains an important need. We report the development of a pulldown-MS proteomic approach, including a custom synthesized non-myristoylated UA-1907-agarose probe, to evaluate the binding selectivity of candidate FAK PPI inhibitors. Melanoma lysates were probed with UA-1907-conjugated agarose beads and eluted associated proteins were analyzed through untagged mass-spectroscopy proteomics. The identified proteins led to the development of a custom focal adhesion (FA) selectivity panel comprised of recombinant VinT, VinH, PARVA, PARVB, Talin-1 Rod 8, and the FAK FAT domain. Surface plasmon resonance (SPR) screening of these FA proteins against UA-1907 determined that only the FAK-FAT domain has a nanomolar binding affinity (K) for UA-1907, whereas other FA proteins have no binding. Overall, we report the development of a customized pulldown-MS approach to characterize PPI drug selectivity that has utility in the FAK drug discovery field. - Source: PubMed
Publication date: 2025/12/14
O'Brien HunterHay BrockSheikh HuzaifahMcCreary LiamParsawar KrishnaMarlowe Timothy - Impaired fear extinction is a hallmark feature of stress- and anxiety-related disorders. Icariin (ICA), a flavonoid derived from Epimedium, exhibits neuroprotective effects in various preclinical models, but its role in fear modulation remains unclear. In this study, we examined the impact of ICA on contextual fear extinction in a rat model subjected to foot shock (FS). Proteomic and metabolomic profiling of the hippocampus was conducted using data-independent acquisition (DIA) proteomics and untargeted metabolomics. ICA treatment significantly enhanced fear extinction in FS-exposed rats. Proteomic analysis identified 175 differentially expressed proteins, with enrichment in platelet activation and extracellular matrix (ECM)-associated pathways. Metabolomic profiling revealed 50 upregulated and 229 downregulated metabolites, highlighting the involvement of the sphingolipid signaling pathway. Among the altered proteins, Myl9, Gp1ba, Parvb, and Prkaca emerged as key candidates implicated in ICA's effects on fear extinction, with Myl9 and Prkaca levels significantly correlated with freezing behavior. Integrative analysis further linked multiple differential metabolites, including (±)12,13-DiHOME, to Myl9 and Prkaca expression. These findings provide novel insights into the molecular mechanisms underlying ICA's therapeutic potential for fear-related neuropsychiatric disorders. - Source: PubMed
Publication date: 2025/09/15
Fan ZhixinYao SimengGong XiayuXu HanfangChen Guangfu - Glioblastoma (GBM) is the most common primary brain cancer, and the prognosis of traditional treatment methods is not favorable. Therefore, we aimed to identify new molecular targets and construct a risk model for GBM diagnosis and prognosis prediction on the basis of neutrophil extracellular trap (NET)-related genes. Gene expression and clinical data were obtained from the TCGA. We constructed a risk model based on four NET-related genes, namely, MAPK1, P2RX1, PARVB and STAT3, using univariate, LASSO and multivariate Cox analyses. The receiver operating characteristic curve analysis with the pROC package revealed that the area under the curve (AUC) values for 1-, 2- and 3-year survival were 0.73, 0.81 and 0.83, respectively. In addition, correlation analysis revealed that MAPK1 expression was negatively correlated with IL15, whereas PARVB, P2RX1 and STAT3 expression levels were positively correlated with IL15, PADI4, CXCL1 and CSF1. In vitro, overexpression of PARVB and P2RX1 STAT3 and the knockdown of MAPK1 promoted the malignant behaviors of GBM cells and activated EMT pathways. Drug sensitivity analysis revealed that STAT3 expression was positively associated with sensitivity to most drugs, whereas MAPK1, PARVB and P2RX1 expression levels were negatively correlated with most drug sensitivity. In conclusion, we identified four NET-related hub genes related to the prognosis of GBM and constructed a risk model with good performance. - Source: PubMed
Publication date: 2025/08/14
Huang ChaoYu Xue-BinZhou Yong-Zhi - This study aimed to identify and characterize novel macrophage-related molecular mechanisms underlying immunosuppression and tumor progression in cervical cancer. Through a systematic integrative analysis guided by immune-related gene signatures and robust regression modeling, we identified PARVB as a novel macrophage-associated prognostic gene with strong predictive value across multiple data sets. Further validation using large-scale transcriptomic data and single-cell RNA-sequencing profiles revealed that PARVB likely activates the SMAD signaling axis, leading to the upregulation of TNFSF13, a key driver of M2 macrophage polarization. This PARVB-SMAD3-TNFSF13 axis enhances interactions between M2 macrophages and TNFSF13 subsets, promoting regulatory T-cell induction and fostering an immunosuppressive tumor microenvironment. Functional assays and multiplex immunohistochemistry further confirmed that this axis drives tumor proliferation and immune evasion. Collectively, our findings uncover a critical PARVB-driven signaling cascade that reprograms macrophages into an immunosuppressive M2 phenotype, facilitating immune escape and cervical cancer progression. Targeting this axis presents a promising therapeutic strategy to reshape the tumor microenvironment and improve immunotherapeutic outcomes. - Source: PubMed
Publication date: 2025/07/29
Guo AihuaYu YilinGuo QinpengZhang EnhuanLin HuaqinFeng MeiZhong PeilinLin JieWang LinghuaLin XiurongWu HaixiaSun Yang - High-risk genes, heterozygous pathogenic mutations of which predispose to familial breast cancers, typically encode factors securing a proper DNA damage response. PALB2 is one such major cellular factor that is needed for alleviation of genomic, replicative, and oxidative stresses. Thus, it has a crucial role in maintaining genomic integrity and protecting cells against cancer. While the malfunctions in DNA damage repair of PALB2-mutated cells have extensively been documented, our research continues to explore cells' other pro-tumorigenic characteristics, focusing particularly on the early stages of malignancy development. Recently, we generated biallelically and monoallelically PALB2-mutated cell lines in a non-malignant background and reported that also their migratory capacity had enhanced together with changes in their transcriptomes and formation of three-dimensionally grown spheroids. Here we demonstrate that JAM3 and PARVB are among the top up-regulated genes in PALB2-mutated cells and that knockdown of the genes reduce migration of the cells and morphological abnormalities of PALB2-mutated spheroids. Macropinocytosis that cancer cells utilize to advance their viability, has also enhanced in PALB2-mutated cells in a β-parvin-dependent manner. Knocking down PALB2 or increased DNA damage did not trigger JAM3 and PARVB expression in control cells, suggesting the need for long-term changes in cell fate and/or cellular conditions. However, DNA damage boosted the nuclear accumulation of a macropinosome marker dextran, indicating that PALB2-mutated cells may use the system to replenish nucleotide stocks for DNA repair. Altogether, several mechanisms can increase the oncogenic potential of PALB2-mutated cells and may offer new approaches to treat PALB2-associated cancers. - Source: PubMed
Publication date: 2025/07/24
Tuppurainen HannaNätynki MarjutLaurila NiinaPylkäs KatriWinqvist RobertPeltoketo Hellevi