{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T16:26:54Z","timestamp":1781108814041,"version":"3.54.1"},"reference-count":0,"publisher":"National Academy of Sciences","issue":"12","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1990,6]]},"abstract":"<jats:p>The invariant chain protein is intracellularly associated with class II major histocompatibility proteins. In many cases, the expression of these molecules appears to be regulated in a similar manner. Contained within the promoter of the invariant chain gene are sequences (X and I gamma 1) that are similar to the X and Y box elements of class II genes, suggesting that these sequences might be involved in its regulation. DNase I footprinting reveals additional cis-acting elements (I gamma 2 and I gamma 3) that contain sequence similarities to NF-kappa B and\/or H2TF1\/KBF1 recognition sequences. A series of fusion constructs with the chloramphenicol acetyltransferase reporter gene were used to analyze the role of these sequences (I gamma 1, I gamma 2, I gamma 3, and X and Y elements) in both normal and mutant B lymphocytes. These data suggest the likelihood of multiple X box proteins in B cells, which can act as both negative and positive regulatory factors.<\/jats:p>","DOI":"10.1073\/pnas.87.12.4590","type":"journal-article","created":{"date-parts":[[2006,5,31]],"date-time":"2006-05-31T07:22:02Z","timestamp":1149060122000},"page":"4590-4594","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":10,"title":["Regulation of the class II-associated invariant chain gene in normal and mutant B lymphocytes."],"prefix":"10.1073","volume":"87","author":[{"given":"C","family":"Doyle","sequence":"first","affiliation":[{"name":"Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P J","family":"Ford","sequence":"additional","affiliation":[{"name":"Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P D","family":"Ponath","sequence":"additional","affiliation":[{"name":"Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T","family":"Spies","sequence":"additional","affiliation":[{"name":"Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J L","family":"Strominger","sequence":"additional","affiliation":[{"name":"Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[1990,6]]},"container-title":["Proceedings of the National Academy of Sciences"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/pnas.org\/doi\/pdf\/10.1073\/pnas.87.12.4590","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,13]],"date-time":"2022-04-13T12:48:05Z","timestamp":1649854085000},"score":1,"resource":{"primary":{"URL":"https:\/\/pnas.org\/doi\/full\/10.1073\/pnas.87.12.4590"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1990,6]]},"references-count":0,"journal-issue":{"issue":"12","published-print":{"date-parts":[[1990,6]]}},"alternative-id":["10.1073\/pnas.87.12.4590"],"URL":"https:\/\/doi.org\/10.1073\/pnas.87.12.4590","relation":{},"ISSN":["0027-8424","1091-6490"],"issn-type":[{"value":"0027-8424","type":"print"},{"value":"1091-6490","type":"electronic"}],"subject":[],"published":{"date-parts":[[1990,6]]},"assertion":[{"value":"1990-06-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}