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The most documented role of SMN, Gemins and UNRIP occurs within the large macromolecular SMN complex and involves the cytoplasmic assembly of spliceosomal uridine\u2010rich small nuclear ribonucleoproteins (UsnRNPs), a housekeeping process critical in all cells. Several reports detailing alternative functions for SMN in either motor neurons or skeletal muscles may, however, hold the answer to the extreme neuromuscular tissue specificity observed in SMA. Recent discoveries indicate that collaboration between SMN and Gemins also extends to these non\u2010canonical functions, hence raising the possibility that mutations in Gemin genes may be the cause of unlinked neuromuscular hereditary syndromes. This review evaluates the functions of Gemins and UNRIP inside the SMN complex and discusses whether these less notorious SMN complex members are capable of acting independently of SMN.<\/jats:p>","DOI":"10.1002\/bies.201000088","type":"journal-article","created":{"date-parts":[[2010,10,15]],"date-time":"2010-10-15T06:56:34Z","timestamp":1287125794000},"page":"1077-1089","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":97,"title":["SMN and Gemins: \u2018We are family\u2019 \u2026 or are we?"],"prefix":"10.1002","volume":"32","author":[{"given":"Ruben 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