AIDA

Last update 08 May 2025

Basic Info

Synonyms

AIDA, Axin interaction partner and dorsalization antagonist, axin interactor, dorsalization associated

+ [3]

Introduction

Acts as a ventralizing factor during embryogenesis. Inhibits axin-mediated JNK activation by binding axin and disrupting axin homodimerization. This in turn antagonizes a Wnt/beta-catenin-independent dorsalization pathway activated by AXIN/JNK-signaling (By similarity).

100 Clinical Results associated with AIDA

100 Translational Medicine associated with AIDA

0 Patents (Medical) associated with AIDA

101

Literatures (Medical) associated with AIDA

01 Mar 2025·Journal of Hazardous Materials

Insertional mutagenesis of AIDA or CYP720B1 in the green alga Chlamydomonas reinhardtii confers copper(II) tolerance and increased biomass

Article

Author: Li, Ya ; Jiang, Lin ; Dong, Zhouzhou ; Wang, Suhui ; Miao, Chenyu ; Wu, Yiqiong ; Qian, Yunyao ; Wang, Liang ; Xu, Chuang

The widespread use of copper (Cu) in industrial and agricultural settings leads to the accumulation of excess Cu within aquatic ecosystems, posing a threat to organism health. Microalgal bioremediation has emerged as a popular and promising solution to mitigate the risks. Nevertheless, the genetic underpinnings and engineering tactics involved in heavy metal bioremediation by microalgae remain inadequately elucidated. In this study, two mutants obtained from screening a Chlamydomonas reinhardtii (C. reinhardtii) mutant library were identified as insertional mutagenesis in the AIDA (Cre12.g487450) and CYP720B1 (Cre10.g426700) genes. Interestingly, these two mutants exhibited decreased cell size and ciliary length but increased cell growth rates. Under Cu(II) stress, the AIDA and CYP720B1 mutants presented dose-dependent tolerance to Cu(II), resulting in increased biomass and improved cellular morphology. Furthermore, the analysis for the antioxidant system suggested that increased Cu(II) tolerance was associated with a low-level response strategy to Cu(II) stress. Transmission electron microscopy images also revealed increased stress-related organelles (starch granules, acidocalcisomes, and plastoglobules) in these two mutants. Considering the excellent Cu(II) tolerance and biomass of these two mutants, our findings provide potential microalgal strains for further genetic modifications and performance mining to improve aquatic Cu(II) bioremediation through biomass enhancement.

09 Jan 2025·Blood

Acute promyelocytic leukemia: long-term outcomes from the HARMONY project

Article

Author: Bullinger, Lars ; Lehmann, Söhren ; Platzbecker, Uwe ; Dillon, Richard ; Ossenkoppele, Gert ; Döhner, Konstanze ; Döhner, Hartmut ; La Sala, Edoardo ; Hernández-Rivas, Jesús María ; Fazi, Paola ; Voso, Maria Teresa ; Giménez, Laura Tur ; Thomas, Ian ; Vignetti, Marco ; Russell, Nigel ; Ramiro, Angela Villaverde ; Gurnari, Carmelo ; Haferlach, Torsten ; Guarnera, Luca ; Piciocchi, Alfonso

AbstractTreatment outcomes for acute promyelocytic leukemia (APL) have improved with the widespread use of targeted therapy with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Our study aimed to validate these data in a large patient cohort, and to redefine prognostic factors. Leveraging the HARMONY Platform, we analyzed 1438 newly diagnosed patients with APL, diagnosed between 1999 and 2022. Patient data derived from the 2 international multicenter Gruppo Italiano Malattie EMatologiche dell’Adulto (GIMEMA)-APL0406 and National Cancer Research Institute (NCRI)-AML17 trials and 4 European registries: the Haemato Oncology Foundation for Adults in the Netherlands, Belgium and Luxembourg (HOVON), AML Study Group (AMLSG), Swedish AML Registry, and Study Alliance Leukemia (SAL). The study cohort included 721 males and 717 females, with a median age of 50.5 years (range, 16-94 years). Of 1309 patients starting therapy, 562 received ATRA-ATO, and 747 idarubicin-based chemotherapy (AIDA-like CHT). Early death (ED) occurred in 85 of 1438 patients (5.9%) at a median of 9 days after APL diagnosis and was independently associated with increasing age and high Sanz risk score (odds ratio [OR], 1.06; 95% confidence interval [CI], 1.04-1.08; and OR, 4.65; 95% CI, 2.55-8.51, respectively). The median follow-up was 5.5 years (interquartile range, 3.2-7.5 years). ATRA-ATO regimen was associated with the best outcome, reaching 91% 7-year overall survival (vs 81% for AIDA-like CHT; hazard ratio [HR], 2.14; 95% CI, 1.51-3.05), 89% event-free survival (vs 71% for AIDA-like CHT; HR, 2.72; 95% CI, 2.01–3.69), and 3% relapse (vs 13% for AIDA-like CHT; HR, 4.19; 95% CI, 2.38-7.39; P < .001 for all outcomes). The survival advantage of ATRA/ATO was independent of patients’ age, Sanz risk score, and treatment scenario. Our study confirms the superiority of ATRA-ATO over ATRA-chemotherapy in patients with APL. Reducing the risk of ED still represents an unmet medical need, in particular in older patients and in high-risk APL.

01 Mar 2023·PLoS genetics

Multimodal CRISPR perturbations of GWAS loci associated with coronary artery disease in vascular endothelial cells.

Article

Author: Lettre, Guillaume ; Lo, Ken Sin ; Fotsing Tadjo, Thierry ; Beaudoin, Mélissa ; Lalonde, Simon ; Wünnemann, Florian ; Kleinstiver, Benjamin P

Genome-wide association studies have identified >250 genetic variants associated with coronary artery disease (CAD), but the causal variants, genes and molecular mechanisms remain unknown at most loci. We performed pooled CRISPR screens to test the impact of sequences at or near CAD-associated genetic variants on vascular endothelial cell functions. Using CRISPR knockout, inhibition and activation, we targeted 1998 variants at 83 CAD loci to assess their effect on three adhesion proteins (E-selectin, ICAM1, VCAM1) and three key endothelial functions (nitric oxide and reactive oxygen species production, calcium signalling). At a false discovery rate ≤10%, we identified significant CRISPR perturbations near 42 variants located within 26 CAD loci. We used base editing to validate a putative causal variant in the promoter of the FES gene. Although a few of the loci include genes previously characterized in endothelial cells (e.g. AIDA, ARHGEF26, ADAMTS7), most are implicated in endothelial dysfunction for the first time. Detailed characterization of one of these new loci implicated the RNA helicase DHX38 in vascular endothelial cell senescence. While promising, our results also highlighted several limitations in using CRISPR perturbations to functionally dissect GWAS loci, including an unknown false negative rate and potential off-target effects.

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