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   https://doi.org/10.1038/s41594-023-01048-x  

   Wilinski, Daniel; Dus, Monica (September 2023, Nature Structural & Molecular Biology)
2. Impact of the Cellular Environment on Adenosine Triphosphate Conformations

   https://doi.org/10.1021/acs.jpclett.2c02375  

   Rickard, Meredith M.; Luo, Haolin; De Lio, Ashley; Gruebele, Martin; Pogorelov, Taras V. (October 2022, The Journal of Physical Chemistry Letters)
3. CD73-Dependent Adenosine Signaling through Adora2b Drives Immunosuppression in Ductal Pancreatic Cancer

   https://doi.org/10.1158/0008-5472.CAN-22-2553  

   Faraoni, Erika Y.; Singh, Kanchan; Chandra, Vidhi; Le Roux, Olivereen; Dai, Yulin; Sahin, Ismet; O'Brien, Baylee J.; Strickland, Lincoln N.; Li, Le; Vucic, Emily; et al (January 2023, Cancer Research)

   Abstract The microenvironment that surrounds pancreatic ductal adenocarcinoma (PDAC) is profoundly desmoplastic and immunosuppressive. Understanding triggers of immunosuppression during the process of pancreatic tumorigenesis would aid in establishing targets for effective prevention and therapy. Here, we interrogated differential molecular mechanisms dependent on cell of origin and subtype that promote immunosuppression during PDAC initiation and in established tumors. Transcriptomic analysis of cell-of-origin–dependent epithelial gene signatures revealed that Nt5e/CD73, a cell-surface enzyme required for extracellular adenosine generation, is one of the top 10% of genes overexpressed in murine tumors arising from the ductal pancreatic epithelium as opposed to those rising from acinar cells. These findings were confirmed by IHC and high-performance liquid chromatography. Analysis in human PDAC subtypes indicated that high Nt5e in murine ductal PDAC models overlaps with high NT5E in human PDAC squamous and basal subtypes, considered to have the highest immunosuppression and worst prognosis. Multiplex immunofluorescent analysis showed that activated CD8+ T cells in the PDAC tumor microenvironment express high levels of CD73, indicating an opportunity for immunotherapeutic targeting. Delivery of CD73 small-molecule inhibitors through various delivery routes reduced tumor development and growth in genetically engineered and syngeneic mouse models. In addition, the adenosine receptor Adora2b was a determinant of adenosine-mediated immunosuppression in PDAC. These findings highlight a molecular trigger of the immunosuppressive PDAC microenvironment elevated in the ductal cell of origin, linking biology with subtype classification, critical components for PDAC immunoprevention and personalized approaches for immunotherapeutic intervention. Significance: Ductal-derived pancreatic tumors have elevated epithelial and CD8+GZM+ T-cell CD73 expression that confers sensitivity to small-molecule inhibition of CD73 or Adora2b to promote CD8+ T-cell–mediated tumor regression. See related commentary by DelGiorno, p. 977 

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4. Conducting Polymer-Based Electrochemical Aptasensor for the Detection of Adenosine

   https://doi.org/10.1021/acsapm.1c01348  

   Runsewe, Damilola O.; Haya, Grace; Betancourt, Tania; Irvin, Jennifer A. (December 2021, ACS Applied Polymer Materials)
5. Mechanisms that Alter Capacity for Adenosine Triphosphate Production and Oxidative Phosphorylation: Insights from Avian Migration

   https://doi.org/10.1093/icb/icae065  

   Hood, Wendy_R (June 2024, Integrative And Comparative Biology)

   Synopsis Avian migration is among the most energetically demanding feats observed in animals. Studies evaluating the physiological underpinnings of migration have repeatedly shown that migratory birds display numerous adaptations that ultimately supply the flight muscle mitochondria with abundant fuel and oxygen during long-distance flights. To make use of this high input, the organs and mitochondria of migrants are predicted to display several traits that maximize their capacity to produce adenosine triphosphate (ATP). This review aims to introduce readers to several mechanisms by which organs and mitochondria can alter their capacity for oxidative phosphorylation and ATP production. The role of organ size, mitochondrial volume, substrate, and oxygen delivery to the electron transport system are discussed. A central theme of this review is the role of changes in electron chain complex activity, mitochondrial morphology and dynamics, and supercomplexes in allowing avian migrants and other taxa to alter the performance of the electron transport system with predictable shifts in demand. It is my hope that this review will serve as a springboard for future studies exploring the mechanisms that alter bioenergetic capacity across animal species. 

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