DLG may refer to:
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USS Coontz (DLG-9/DDG-40) was a Farragut-class destroyer leader/frigate in the United States Navy. She was named after Admiral Robert Coontz, the US Navy's second chief of naval operations.
Commissioned in 1960, she spent the early part of her career in the Pacific Ocean, participating in four tours of duty during the Vietnam War. In the early 1970s she transferred to the east coast and spent the remainder of her service years in the Caribbean Sea, Atlantic Ocean, Mediterranean Sea, and Persian Gulf. She assisted in saving USS Stark after that ship was hit by Iraqi missiles. In 1975, as part of the Navy's reclassification process, all ships of her class were reclassified as guided missile destroyers (DDG).
Coontz was decommissioned in 1989, and sold for scrap five years later. Her transom nameplate was salvaged and donated to the city of Hannibal, Missouri, birthplace of Admiral Coontz.
Coontz's keel was laid at Puget Sound Naval Shipyard in March 1957, 39 years after Admiral Coontz left his post as the shipyard's commander. The first guided-missile frigate to be built on the West Coast, and the second ship to bear the name of the Navy’s second chief of naval operations, Coontz was christened by Mrs. Robert J. Coontz, wife of the admiral’s grandson, on 6 December 1958.
Disks large homolog 2 (DLG2) also known as channel-associated protein of synapse-110 (chapsyn-110) or postsynaptic density protein 93 (PSD-93) is a protein that in humans is encoded by the DLG2 gene.
Chapsyn-110/PSD-93 a member of the membrane-associated guanylate kinase (MAGUK) family. The protein forms a heterodimer with a related family member that may interact at postsynaptic sites to form a multimeric scaffold for the clustering of receptors, ion channels, and associated signaling proteins. Alternatively spliced transcript variants encoding distinct isoforms have been described but their full-length nature has yet to be completely determined.
Model organisms have been used in the study of DLG2 function. A knockout mouse line, called Dlg2tm1Dsb was generated. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Twenty four tests were carried out on homozygous mutant mice and five significant abnormalities were observed. Both sexes had atypical indirect calorimetry and DEXA parameters. Females also had decreased body weight, decreased circulating HDL cholesterol levels, and increased susceptibility to bacterial infection.