{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T11:21:45Z","timestamp":1790680905124,"version":"4.1.0"},"reference-count":59,"publisher":"American Society of Hematology","issue":"5","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,3,1]]},"abstract":"<jats:p>Acute promyelocytic leukemia (APL) is always associated with chromosomal translocations that disrupt the retinoic acid receptor \u03b1 (RAR\u03b1) gene. Whether these translocations relate to a role for endogenous RAR\u03b1 in normal granulopoiesis remains uncertain because most studies addressing this question have used non-physiological overexpression systems. Granulocyte differentiation in cells derived from RAR\u03b1-deficient (RAR\u03b1\u2212\/\u2212) mice was studied and evaluated in the context of agonist-bound and ligand-free RAR\u03b1. Our results demonstrate that RAR\u03b1 is dispensable for granulopoiesis, as RAR\u03b1\u2212\/\u2212 mice have a normal granulocyte population despite an impaired ability to respond to retinoids. However, although it is not absolutely required, RAR\u03b1 can bidirectionally modulate granulopoiesis. RAR\u03b1 stimulates differentiation in response to exogenous retinoic acid. Furthermore, endogenous retinoids control granulopoiesis in vivo, as either vitamin A\u2013deficient mice or animals treated with an RAR antagonist accumulate more immature granulocytes in their bone marrow. Conversely, RAR\u03b1 acts to limit differentiation in the absence of ligand because granulocyte precursors from RAR\u03b1\u2212\/\u2212 mice differentiate earlier in culture. Thus, the block in granulopoiesis exerted by RAR\u03b1 fusion proteins expressed in APL cells may correspond to an amplification of a normal function of unliganded RAR\u03b1.<\/jats:p>","DOI":"10.1182\/blood.v97.5.1314","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T12:46:47Z","timestamp":1027774007000},"page":"1314-1320","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":116,"title":["Positive and negative regulation of granulopoiesis by endogenous RAR\u03b1"],"prefix":"10.1182","volume":"97","author":[{"given":"Philippe","family":"Kastner","sequence":"first","affiliation":[{"name":"From the Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, Illkirch, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. Jeffrey","family":"Lawrence","sequence":"additional","affiliation":[{"name":"From the Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, Illkirch, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caroline","family":"Waltzinger","sequence":"additional","affiliation":[{"name":"From the Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, Illkirch, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norbert B.","family":"Ghyselinck","sequence":"additional","affiliation":[{"name":"From the Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, Illkirch, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre","family":"Chambon","sequence":"additional","affiliation":[{"name":"From the Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, Illkirch, 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