Antarctic Survey Telescope 3-3: Overview, System Performance and Preliminary Observations at Yaoan, Yunnan

The third Antarctic Survey Telescope array instrument at Dome A in Antarctica, the AST3-3 telescope, has been in commissioning from March 2021. We deployed AST3-3 at the Yaoan astronomical station in Yunnan Province for an automatic time-domain survey and follow-up observations with an optimised observation and protection system. The telescope system of AST3-3 is similar to that of AST3-1 and AST3-2, except that it is equipped with a 14K~$\times$~10K QHY411 CMOS camera. AST3-3 has a field of view of $1.65^\circ \times 1.23^\circ$ and is currently using the $g$ band filter. During commissioning at Yaoan, AST3-3 aims to conduct an extragalactic transient survey, coupled with prompt follow-ups of opportunity targets. In this paper, we present the architecture of the AST3-3 automatic observation system. We demonstrate the data processing of observations by representatives SN 2022eyw and GRB 210420B.Comment: 20 pages, 15 figure

Classification in cryo-electron tomograms

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Kisspeptin-10 binding to Gpr54 in osteoclasts prevents bone loss by activating Dusp18-mediated dephosphorylation of Src

Abstract Osteoclasts are over-activated as we age, which results in bone loss. Src deficiency in mice leads to severe osteopetrosis due to a functional defect in osteoclasts, indicating that Src function is essential in osteoclasts. G-protein-coupled receptors (GPCRs) are the targets for ∼35% of approved drugs but it is still unclear how GPCRs regulate Src kinase activity. Here, we reveal that GPR54 activation by its natural ligand Kisspeptin-10 (Kp-10) causes Dusp18 to dephosphorylate Src at Tyr 416. Mechanistically, Gpr54 recruits both active Src and the Dusp18 phosphatase at its proline/arginine-rich motif in its C terminus. We show that Kp-10 binding to Gpr54 leads to the up-regulation of Dusp18. Kiss1, Gpr54 and Dusp18 knockout mice all exhibit osteoclast hyperactivation and bone loss, and Kp-10 abrogated bone loss by suppressing osteoclast activity in vivo. Therefore, Kp-10/Gpr54 is a promising therapeutic target to abrogate bone resorption by Dusp18-mediated Src dephosphorylation