Last update 01 Nov 2024

ADA2

Last update 01 Nov 2024

Basic Info

Synonyms

ADA2, adenosine deaminase 2, ADGF

+ [3]

Introduction

Adenosine deaminase that may contribute to the degradation of extracellular adenosine, a signaling molecule that controls a variety of cellular responses. Requires elevated adenosine levels for optimal enzyme activity. Binds to cell surfaces via proteoglycans and may play a role in the regulation of cell proliferation and differentiation, independently of its enzyme activity.

100 Clinical Results associated with ADA2

100 Translational Medicine associated with ADA2

0 Patents (Medical) associated with ADA2

643

Literatures (Medical) associated with ADA2

01 Dec 2024·Plant Science

Overexpression of GmSRC2 confers resistance to Phytophthora sojae in soybean

Article

Author: Sun, Ruidong ; Wang, Haitang ; Zhao, Jinming ; Deng, Sushuang ; Xing, Han ; Gou, Han ; Guo, Na ; Fang, Xiaowan ; Xuan, Huidong ; Zhang, Yu

Phytophthora root and stem rot caused by Phytophthora sojae (P. sojae) is one of the most destructive diseases to affect soybean (Glycine max (L.) Merr) production. GmSRC2 that encodes a C2 domain-containing protein can respond to various stresses, however, the molecular mechanism of GmSRC2 in resistance of soybean to P. sojae is yet to be fully elucidated. In this study, GmSRC2 was found to be significantly up-regulated under P. sojae treatment; GmSRC2-overexpression (OE) transgenic lines and GmSRC2-silencing transient plants were generated via Agrobacterium tumefaciens mediated transformation and virus-induced gene silencing (VIGS) system, respectively. Infected leaves and cotyledons of OE-GmSRC2-1 and OE-GmSRC2-2 lines showed significant decreases in the disease symptoms and P. sojae biomass than those of wild type (WT); the activities of superoxide dismutase (SOD) and peroxidase (POD) confirmed the accumulation of reactive oxygen species (ROS) in overexpressed transgenic lines. Whereas, silencing of GmSRC2 severely increased the disease symptoms and the biomass of P. sojae. Further, we confirmed that GmSRC2 interacted with the effector PsAvh23 of P. sojae, and the C2 domain was crucial for the interaction. Overexpression of GmSRC2 upregulated the ADA2/GCN5 module upon P. sojae. The aforementioned results demonstrated that GmSRC2 played vital roles in regulating soybean resistance to oomycetes.

01 Nov 2024·Cell Reports

ADA2 is a lysosomal deoxyadenosine deaminase acting on DNA involved in regulating TLR9-mediated immune sensing of DNA

Article

Author: Smulski, Cristian R. ; Grimbacher, Bodo ; Trompouki, Eirini ; Goschin, Andreas ; Seidl, Maximilian ; Abdullah, Zeinab ; Bartok, Eva ; Dominick, Felix Immunuel ; Peng, Xiao P ; Smulski, Cristian R ; Latz, Eicke ; Greiner-Tollersrud, Ole Kristian ; Spahiu, Ambra ; Polyzou, Aikaterini ; Huebscher, Katrin ; Peng, Xiao P. ; Hartmann, Gunther ; Boehler, Vincent ; Sogkas, Georgios ; Andryka-Cegielski, Katarzyna ; Proietti, Michele ; Vågbø, Cathrine ; Link, Regina ; Staab, Dieter ; Srinivas, Honnappa ; Baasch, Sebastian ; Alseth, Ingrun ; Krausz, Máté ; Marchant, Martine ; Henneke, Philippe ; Guerini, Danilo ; Warncke, Max ; Geiger, Roger ; Ebersbach, Hilmar

Although adenosine deaminase 2 (ADA2) is considered an extracellular ADA, evidence questions the physiological relevance of this activity. Our study reveals that ADA2 localizes within the lysosomes, where it is targeted through modifications of its glycan structures. We show that ADA2 interacts with DNA molecules, altering their sequences by converting deoxyadenosine (dA) to deoxyinosine (dI). We characterize its DNA substrate preferences and provide data suggesting that DNA, rather than free adenosine, is its natural substrate. Finally, we demonstrate that dA-to-dI editing of DNA molecules and ADA2 regulate lysosomal immune sensing of nucleic acids (NAs) by modulating Toll-like receptor 9 (TLR9) activation. Our results describe a mechanism involved in the complex interplay between NA metabolism and immune response, possibly impacting ADA2 deficiency (DADA2) and other diseases involving this pathway, including autoimmune diseases, cancer, or infectious diseases.

01 Oct 2024·Journal of Clinical Immunology

Genetic Testing in Patients with Autoimmune Lymphoproliferative Syndrome: Experience of 802 Patients at Cincinnati Children’s Hospital Medical Center

Article

Author: Wu, Yaning ; Guan, Qiaoning ; Xu, Xinxiu ; Liu, Jie ; Bleesing, Jack ; Denton, James ; Dawson, D Brian ; Zhang, Wenying

AbstractAutoimmune lymphoproliferative syndrome (ALPS) is a rare genetic disorder featuring chronic lymphadenopathy, splenomegaly, cytopenias, and increased lymphoma risk. Differentiating ALPS from immunodeficiencies with overlapping symptoms is challenging. This study evaluated the performance and the diagnostic yield of a 15-gene NGS panel for ALPS at Cincinnati Children’s Hospital Medical Center. Samples from 802 patients submitted for ALPS NGS panel were studied between May 2014 and January 2023. A total of 62 patients (7.7%) had a definite diagnosis: 52/62 cases (84%) showed 37 unique pathogenic/likely pathogenic germline FAS variants supporting ALPS diagnosis (6.5%, 52/802). The ALPS diagnostic yield increased to 30% in patients who additionally fulfilled abnormal ALPS immunology findings criteria. 17/37 (46%) diagnostic FAS variants were novel variants reported for the first time in ALPS. 10/802 cases (1.2%) showed diagnostic findings in five genes (ADA2, CTLA4, KRAS, MAGT1, NRAS) which are related to autoimmune lymphoproliferative immunodeficiency (ALPID). Family studies enabled the reclassification of variants of unknown significance (VUS) and also the identification of at-risk family members of FAS-positive patients, which helped in the follow-up diagnosis and treatment. Alongside family studies, complete clinical phenotypes and abnormal ALPS immunology and Fas-mediated apoptosis results helped clarify uncertain genetic findings. This study describes the largest cohort of genetic testing for suspected ALPS in North America and highlights the effectiveness of the ALPS NGS panel in distinguishing ALPS from non-ALPS immunodeficiencies. More comprehensive assessment from exome or genome sequencing could be considered for undefined ALPS-U patients or non-ALPS immunodeficiencies after weighing cost, completeness, and timeliness of different genetic testing options.

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