DAB2IP antibody
- Known as:
- DAB2IP (anti-)
- Catalog number:
- orb101664
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- DAB2IP antibody
Related genes to: DAB2IP antibody
- Gene:
- DAB2IP NIH gene
- Name:
- DAB2 interacting protein
- Previous symbol:
- -
- Synonyms:
- AF9Q34, DIP1/2, KIAA1743, AIP1
- Chromosome:
- 9q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-23
- Date modifiied:
- 2016-10-05
Related products to: DAB2IP antibody
Related articles to: DAB2IP antibody
- In advanced Prostate Cancer (PCa), metastatic spread and the inevitable emergence of enzalutamide resistance represent major clinical hurdles. Although apolipoprotein L3 (APOL3) is linked to oncogenesis, its precise mechanistic role in PCa progression and antiandrogen resistance, particularly its regulation of the STAT3-DAB2IP axis, remains largely unexplored. - Source: PubMed
Publication date: 2026/05/25
Wang QuanxinZuo SonglinChen LinWan FangningHong ZheXu WenhaoHou WentingYe Dingwei - The 2025 World Allergy Organization (WAO) Guidelines for the Classification, Diagnosis, and Treatment of Hereditary Angioedema (HAE) with Consideration of Worldwide Disparities provide a comprehensive, evidence-informed, and globally applicable framework for the care of this rare and potentially life-threatening disorder. HAE is a genetic disease characterized by recurrent episodes of subcutaneous and submucosal swelling, most commonly mediated by bradykinin, and is associated with substantial morbidity, impaired quality of life, and a lifelong risk of fatal laryngeal edema. The Guidelines were developed by an international panel of 40 experts from 22 countries, with representation from all world regions, reflecting the commitment of WAO to geographic diversity, inclusiveness, and global relevance. The development process for these guidelines followed a structured and transparent methodology that integrated systematic literature review, appraisal of real-world evidence, and application of the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework adapted for rare diseases, complemented by a formal Delphi consensus process. This approach was specifically designed to address the limitations of conventional evidence hierarchies in rare disorders, while ensuring clinical applicability across heterogeneous healthcare systems and resource settings. A central element of the guidelines is an updated classification of HAE based on underlying pathophysiology and disease endotypes. The traditional distinction between HAE types 1 and 2 is unified under the term HAE with C1 inhibitor deficiency (HAE-C1-INH), reflecting shared biological mechanisms and management principles. The guidelines also recognize an expanding spectrum of HAE with normal C1 inhibitor (HAE-nC1-INH), including forms associated with pathogenic variants in F12, PLG, ANGPT1, KNG1, MYOF, HS3ST6, CPN1, and DAB2IP, as well as cases with currently unidentified genetic causes. The diagnostic strategy emphasizes early clinical recognition based on characteristic features, including recurrent angioedema without urticaria, abdominal or laryngeal involvement, early symptom onset, and family history. A simplified diagnostic algorithm is proposed, prioritizing the C1 inhibitor functional assay as the preferred initial test when performed in a reliable specialized laboratory. Alternative diagnostic pathways are outlined for settings with limited access to specialized testing, including pragmatic combinations of biochemical assays and selective use of genetic testing, particularly relevant for HAE-nC1-INH and family screening. Management recommendations address on-demand treatment of acute attacks, short-term prophylaxis, and individualized long-term prophylaxis. Universal access to on-demand therapy is emphasized for all patients with confirmed HAE, including those who are asymptomatic, given the unpredictable nature of attacks and lifelong risk. Long-term prophylaxis is addressed within a treat-to-target framework aimed at achieving complete disease control and sustained improvement in health-related quality of life, with regular reassessment and shared decision-making. Empowering patients and caregivers through structured education, access to appropriate medications, and integration with specialized referral centers is associated with earlier treatment, reduced healthcare utilization, and improved equity of care and reduced avoidable morbidity and mortality worldwide. The 2025 WAO Guidelines for Hereditary Angioedema establish an evidence-informed, patient-centered, and forward-looking framework for the classification, diagnosis, and management of HAE. By integrating advances in pathophysiology, diagnostics, and therapeutics with global expert consensus and real-world considerations, the guidelines aim to support consistent, equitable, and high-quality care for patients with HAE across regions and healthcare systems. - Source: PubMed
Publication date: 2026/03/19
Vázquez Daniel OGiavina-Bianchi PedroJosviack DaríoKaplan Allen PMartinez Pablo A SFantini ClaudioBernstein Jonathan AAbbas ShahidLevin Nancy AgmonAl-Ahmad MonaAlandijani SultanAlhashmi Hani AbdullahAli Ramzy MohammedAllam InesAl-Nesf Al-Mansouri MaryamAl-Tamemi SalemAltrichter SabineCastelló Mirta ÁlvarezAndoh Hilary DAun Marcelo VivoloMapondela Kassim BabuBanerji AleenaBara Noémi-AnnaBarrera Olga MelcinaPerigault Paulo BarreraBranco-Ferreira ManuelCalderón-Llosa Oscar ManuelCanonica Giorgio WalterAlmarales Raúl CastroCecchi LorenzoChang Yoon-SeokChantaphakul HiroshiChikovani TinatinChong-Neto Herberto JoseContreras-Verduzco Francisco AlbertoDefendi FedericaDorsainvil VilbrunEbisawa MotohiroEl-Sayed Zeinab AFasano Mary BethFazlollahi Mohammad RezaFemine EuguensFernandes Fátima RodriguesFiocchi AlessandroFonacier LuzGallego ClaudiaGarcía Abujeta José LuisGereda José EnriqueGiordano ErminiaGökmen Nihal MeteGómez R MaximilianoGonzalez MonicaDíaz Sandra GonzálezGrau MasumiHakl RomanHide MichihiroHossny ElhamHuilaja LauraHuq Syed RezaulIrani CarlaIshchanka AksanaIspayeva ZhanatJamalyan Kristina RKaidashev IgorKamkamidze GeorgeTanno Luciana KaseKathuria P CKessel AharonKiani-Alikhan SorenaKomarla Nagendra PrasadKvedarienė VioletaLang David MLee Yong WonLevin MichaelLi Philip HLi HenryLumry William RMachavariani KetevanMartinez-Sager InmaculadaMaselli Juan PMikos NikolaosMitskevich NunuMobayed Hassan M SMonge Ortega Olga PatriciaMorita HideakiMunkhbayarlakh SonomjamtsNabavi MohammadNaqvi Muhammad RazaOcampo JaimeOlivares MargaritaOrtega-Martell Jose AntonioOyuntsatsral BatsaikhanPapadopoulos NikosPatella VincenzoPawankar RubyPeter JonnyPsarros FotisRegateiro FredericoReidl MarcRigalt Ann MRincón Fernández Jenny MarielRivera Gómez Maria AntoniaRojo Gutiérrez María IsabelSahiner Ümit MuratSandoval-Ruballos MónicaSantos NatachaSarrazola MauricioSchrijvers RikShchurok IrynaSheikh Farrukh RafiqueSobotkova MartaSoria AngeleStefanaki EfthaliaTarazona RobinLuján Alejandra ValecillosRostan Marylin ValentinValerieva AnnaWing-Kin Wong GaryYong Patrick F KZaitoun FaresMartin Bryan LAnsotegui Ignacio JMorais-Almeida MárioCraig Timothy J - Down syndrome (DS), caused by trisomy 21, confers a near-universal risk for Alzheimer's disease (AD), yet individuals exhibit marked variability in cognitive decline, suggesting the presence of cellular mechanisms that modulate vulnerability and resilience. However, these mechanisms remain poorly defined in the human brain. Here, we integrate matched single-nucleus RNA-seq and ATAC-seq profiles from the prefrontal cortex (PFC) and amygdala (AMY) of age-matched individuals with DS with and without AD (DSAD), enabling direct comparison within a shared genetic background. We identify basal astrocytes in the PFC as a selectively vulnerable cell state in DSAD, characterized by both reduced abundance and coordinated transcriptional and regulatory reprogramming. This state exhibits a shift away from homeostatic support functions, with decreased cytokine signaling and lipid-handling programs, alongside increased steroid- and nuclear receptor-associated activity. Concomitantly, chromatin accessibility profiling reveals reduced engagement of immune- and stress-responsive transcription factor programs, including AP-1, STAT, and BACH families, with linked regulatory perturbations at loci such as ABCA1, DAB2IP, and IL1RAP. Together, these findings define a previously unrecognized astrocyte state marked by epigenetic constraint and diminished responsiveness to stress and inflammatory signals, distinguishing it from classical reactive astrocyte phenotypes. Our results nominate PFC basal astrocytes as a key locus of vulnerability in DSAD and suggest that failure to mount appropriate astrocyte responses, rather than overt activation alone, may contribute to neurodegenerative progression. - Source: PubMed
Publication date: 2026/04/21
Sun ChuhanwenThomas RainaStringer CherieGalani KyriakitsaHo Li-LunSun NaRenfro AshleyWright SierraFirenze RosalindTsai Li-HueiHead ElizabethKellis ManolisYang Jiekun - Group 3 innate lymphoid cells (ILC3s) preserve intestinal barrier integrity by producing IL-22 and IL-17A, yet the molecular mechanisms that maintain these cytokines during inflammation are incompletely defined. Here, we identify DAB2IP as a cell-intrinsic regulator of ILC3 effector function. In human inflammatory bowel disease mucosa, DAB2IP expression is reduced and associated with transcriptional programs linked to impaired epithelial repair. In murine models, inflammatory cues dynamically modulate Dab2ip in ILC3s, and genetic loss of DAB2IP diminishes IL-22 and IL-17A, compromising host defense during Citrobacter rodentium infection, and exacerbates dextran sulfate sodium-induced colitis. Mechanistically, DAB2IP enables efficient NF-κB activation, promoting IκBα degradation, p65 nuclear accumulation, and thus transcription of Il22/Il17a and NF-κB targets. These results reveal a context-dependent role for DAB2IP as a positive regulator of NF-κB in ILC3s, highlighting its previously unknown function in mucosal immunity and epithelial repair, and suggesting that restoring DAB2IP signaling could enhance barrier protection during intestinal inflammation. - Source: PubMed
Liu LiangDavidorf BenjaminDong PeixianYu JohnHo DavidZhang BingHe Zhiheng - Metastasis, the colonization of distant organs by cells derived from primary cancer, is the leading cause of mortality in pancreatic adenocarcinoma (PAAD). Growing evidence indicates that cancer-derived exosomes play pivotal roles in facilitating cancer metastasis by promoting pre-metastatic niche formation. However, the contribution of PAAD-derived exosomal microRNAs (MiRNAs) to this process remains poorly characterized. In this study, we identified specific PAAD-derived exosomal miRNAs involved in metastatic progression. Sequencing of small RNAs extracted from circulating exosomes derived from patients with metastatic or non-metastatic PAAD revealed that miR-92a-3p is associated with a metastatic phenotype. We demonstrated that exosomal miR-92a-3p facilitates cancer cells' extravasation and lung metastasis by disrupting vascular barrier integrity. Mechanistically, exosomal miR-92a-3p directly inhibits the tumor suppressor disabled homolog 2 interacting protein (DAB2IP), thereby activating the PI3K-AKT signaling cascade in endothelial cells (ECs). This activation attenuates expression of intracellular junction markers and stimulates endothelial nitric oxide synthase, leading to increased vascular permeability. Our findings suggest that targeting miR-92a-3p could represent a potential strategy to reduce metastasis in PAAD. - Source: PubMed
Publication date: 2026/04/08
Li LuhanCui YanyanZhang MiaoShen TianyuWang DekunMi XueZhang YuyingTan XiaoyueVaquero AlejandroBraun ThomasHao JihuiIanni AlessandroJiang ChunyangYue Shijing