{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T18:37:59Z","timestamp":1792780679213,"version":"4.5.0"},"reference-count":16,"publisher":"Public Library of Science (PLoS)","issue":"10","license":[{"start":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T00:00:00Z","timestamp":1792713600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Beijing Hospital Authority Mission Plan","award":["SML20191101"],"award-info":[{"award-number":["SML20191101"]}]},{"name":"Science Foundation of Peking University Cancer Hospital","award":["2022-8"],"award-info":[{"award-number":["2022-8"]}],"id":[{"id":"https:\/\/ror.org\/00nyxxr91","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS One"],"abstract":"<jats:p>\n                    The\n                    <jats:italic>TTC22<\/jats:italic>\n                    gene encodes a protein containing seven tetratricopeptide repeats (TPRs), which mediate protein\u2012protein interactions as chaperones. We previously reported that the level of\n                    <jats:italic>TTC22<\/jats:italic>\n                    transcript variant 1 (\n                    <jats:italic>TTC22v1<\/jats:italic>\n                    ) was downregulated in human colon adenocarcinoma (COAD) and that TTC22 upregulated m6A-mediated\n                    <jats:italic>WTAP<\/jats:italic>\n                    and\n                    <jats:italic>SNAI1<\/jats:italic>\n                    expression via the TTC22\u2012RPL4 interaction and subsequently promoted COAD metastasis. Thus, a commercially available C57BL\/6N mouse model in which the\n                    <jats:italic>Ttc22<\/jats:italic>\n                    exon 2&amp;3 encoding the TPR4 (equal to the human TTC22 TPR3) domain was knocked out via CRISPR-Cas9 was used to evaluate the contribution of\n                    <jats:italic>Ttc22<\/jats:italic>\n                    to the development of mice and COAD. To determine the status of Ttc22 expression in\n                    <jats:italic>Ttc22<\/jats:italic>\n                    knockout mice, we prepared a rabbit polyclonal antibody against the mouse Ttc22 protein, which could bind both wild-type Ttc22 and TPR4-deleted Ttc22 proteins overexpressed in HEK293T cells, as determined by Western blot analysis. Ttc22 proteins were detected in colon tissue samples from wild-type mice and\n                    <jats:italic>Ttc22<\/jats:italic>\n                    hemi-knockout (\n                    <jats:italic>Ttc22<\/jats:italic>\n                    <jats:sup>+\/-<\/jats:sup>\n                    ) mice but not in those from fully\n                    <jats:italic>Ttc22<\/jats:italic>\n                    knockout (\n                    <jats:italic>Ttc22<\/jats:italic>\n                    <jats:sup>-\/-<\/jats:sup>\n                    ) mice. Unfortunately, the long-term observation results demonstrated that\n                    <jats:italic>Ttc22<\/jats:italic>\n                    knockout (KO, including\n                    <jats:italic>Ttc22<\/jats:italic>\n                    <jats:sup>+\/-<\/jats:sup>\n                    or\n                    <jats:italic>Ttc22<\/jats:italic>\n                    <jats:sup>-\/-<\/jats:sup>\n                    ) did not affect the body weight, development, fertility, or spontaneous tumor incidence of male or female mice. No differences in the incidence of AOM\/DSS-induced COAD were observed between these mouse groups, although\n                    <jats:italic>Ttc22<\/jats:italic>\n                    deletion partially resulted in the upregulation of genes related to the host adaptive response to inflammation in the colon mucosa. In conclusion, no phenotypes were induced by\n                    <jats:italic>Ttc22<\/jats:italic>\n                    inactivation in C57BL\/6N mice.\n                  <\/jats:p>","DOI":"10.1371\/journal.pone.0361340","type":"journal-article","created":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T17:42:09Z","timestamp":1792777329000},"page":"e0361340","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":0,"title":["No phenotypes in Ttc22 knockout mice"],"prefix":"10.1371","volume":"21","author":[{"given":"Jiaoyang","family":"Liu","sequence":"first","affiliation":[{"name":"Peking University Cancer Hospital and Institute","place":["Beijing, China"],"department":["Key Laboratory of Carcinogenesis and Translational Research (MOE\/Beijing), Division of Etiology"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liankun","family":"Gu","sequence":"additional","affiliation":[{"name":"Peking University Cancer Hospital and Institute","place":["Beijing, China"],"department":["Key Laboratory of Carcinogenesis and Translational Research (MOE\/Beijing), Division of Etiology"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abin","family":"You","sequence":"additional","affiliation":[{"name":"Peking University Cancer Hospital and Institute","place":["Beijing, China"],"department":["Key Laboratory of Carcinogenesis and Translational Research (MOE\/Beijing), Division of Etiology"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongfan","family":"Yuan","sequence":"additional","affiliation":[{"name":"Peking University Cancer Hospital and Institute","place":["Beijing, China"],"department":["Key Laboratory of Carcinogenesis and Translational Research (MOE\/Beijing), Division of Etiology"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Zhou","sequence":"additional","affiliation":[{"name":"Peking University Cancer Hospital and Institute","place":["Beijing, China"],"department":["Key Laboratory of Carcinogenesis and Translational Research (MOE\/Beijing), Division of Etiology"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Tian","sequence":"additional","affiliation":[{"name":"Peking University Cancer Hospital and Institute","place":["Beijing, China"],"department":["Key Laboratory of Carcinogenesis and Translational Research (MOE\/Beijing), Division of Etiology"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5161-5943","authenticated-orcid":true,"given":"Dajun","family":"Deng","sequence":"additional","affiliation":[{"name":"Peking University Cancer Hospital and Institute","place":["Beijing, China"],"department":["Key Laboratory of Carcinogenesis and Translational Research (MOE\/Beijing), Division of 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