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Signal."],"published-print":{"date-parts":[[2023,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Matricellular proteins comprise several families of secreted proteins that function in higher animals at the interface between cells and their surrounding extracellular matrix. Targeted gene disruptions that result in loss of viability in mice have revealed critical roles for several matricellular proteins in murine embryonic development, including two members of the cellular communication network (CCN) gene family. In contrast, mice lacking single or multiple members of the thrombospondin (THBS) gene family remain viable and fertile. The frequency of loss of function mutants, identified using human deep exome sequencing data, provided evidence that some of the essential genes in mice, including\n                    <jats:italic>Ccn1<\/jats:italic>\n                    , are also essential genes in humans. However, a deficit in loss of function mutants in humans indicated that\n                    <jats:italic>THBS1<\/jats:italic>\n                    is also highly loss-intolerant. In addition to roles in embryonic development or adult reproduction, genes may be loss-intolerant in humans because their function is needed to survive environmental stresses that are encountered between birth and reproduction. Laboratory mice live in a protected environment that lacks the exposures to pathogens and injury that humans routinely face. However, subjecting\n                    <jats:italic>Thbs1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice to defined stresses has provided valuable insights into functions of thrombospondin-1 that could account for the loss-intolerance of\n                    <jats:italic>THBS1<\/jats:italic>\n                    in humans.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Graphical Abstract<\/jats:bold>\n                  <\/jats:p>","DOI":"10.1007\/s12079-023-00722-5","type":"journal-article","created":{"date-parts":[[2023,1,23]],"date-time":"2023-01-23T06:02:56Z","timestamp":1674453776000},"page":"485-493","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Why do humans need thrombospondin-1?"],"prefix":"10.1002","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0513-6225","authenticated-orcid":false,"given":"Sukhbir","family":"Kaur","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2481-2981","authenticated-orcid":false,"given":"David D.","family":"Roberts","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2023,1,23]]},"reference":[{"key":"722_CR1","doi-asserted-by":"publisher","first-page":"92","DOI":"10.1016\/j.ajhg.2010.12.002","volume":"88","author":"H Abouzeid","year":"2011","unstructured":"Abouzeid H, Boisset G, Favez T, Youssef M, Marzouk I, Shakankiry N, Bayoumi N, Descombes P, Agosti C, Munier FL, Schorderet DF (2011) Mutations in the SPARC-related modular calcium-binding protein 1 gene, SMOC1, cause waardenburg anophthalmia syndrome. 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