{"id":{"repo_id":"tenn-hsc","oai_identifier":"oai:dc.uthsc.edu:dissertations-1113"},"canonical_url":"https://search.dev.ndltd.org/etd/tenn-hsc/oai:dc.uthsc.edu:dissertations-1113","repository":{"repo_id":"tenn-hsc","name":"University of Tennessee Health Science Center","base_url":"https://dc.uthsc.edu/do/oai/"},"display":{"title":"Preliminary Study on How Tumor Suppressor Nf2 Inhibits Transcriptional Coactivators Yap/Taz in the Developing Mouse Brain","abstract":"<p>Normal brain development requires precise coordination of neural progenitor proliferation and differentiation, the mechanism of which is not well known. Recently the tumor suppressor neurofibromatosis 2 (Nf2) was shown to regulate the balance of neural progenitor proliferation and differentiation in the developing mouse brain through the Hippo pathway effectors, transcriptional coactivators Yap/Taz. The molecular mechanism of how Nf2 regulates Yap/Taz is not understood. Here I showed that Nf2 regulated the Yap/Taz activity by decreasing the stability of Yap/Taz. The regulation was independent of Yap-S366 phosphorylation, which is required for Yap degradation. I also showed that Nf2 did not regulate Lats1/2 kinases activity. Finally I found Nf2 interacted with Yap in mouse embryonic brain and identified the domains that were required for Nf2-Yap interaction. My study suggests that Nf2 may regulate Yap/Taz independent of the canonical Hippo pathway in the developing mammalian brain. </p>","abstract_html":"&lt;p&gt;Normal brain development requires precise coordination of neural progenitor proliferation and differentiation, the mechanism of which is not well known. Recently the tumor suppressor neurofibromatosis 2 (Nf2) was shown to regulate the balance of neural progenitor proliferation and differentiation in the developing mouse brain through the Hippo pathway effectors, transcriptional coactivators Yap/Taz. The molecular mechanism of how Nf2 regulates Yap/Taz is not understood. Here I showed that Nf2 regulated the Yap/Taz activity by decreasing the stability of Yap/Taz. The regulation was independent of Yap-S366 phosphorylation, which is required for Yap degradation. I also showed that Nf2 did not regulate Lats1/2 kinases activity. Finally I found Nf2 interacted with Yap in mouse embryonic brain and identified the domains that were required for Nf2-Yap interaction. My study suggests that Nf2 may regulate Yap/Taz independent of the canonical Hippo pathway in the developing mammalian brain. &lt;/p&gt;","abstract_has_math":false,"creators":["He, Yu"],"institution":null,"degree_name":"Master of Science (MS)","degree_level":"Thesis","degree_discipline":"Biomedical Sciences","degree_department":null,"school":null,"contributors":["Xinwei Cao, Ph.D."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2014,"date_issued":"2014-05-01T07:00:00Z","date_published":"2014-05-01T07:00:00Z","updated_at":"2026-07-24T05:00:11Z","subjects":["Brain development","Hippo signaling","Nf2/Merlin","Yap/Taz","Medical Sciences","Medicine and Health Sciences","Neurosciences"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://dc.uthsc.edu/dissertations/105","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Xinwei Cao, Ph.D."]},{"key":"dc:creator","label":"Author","values":["He, Yu"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2016-06-07T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biomedical Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (MS)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Brain development","Hippo signaling","Nf2/Merlin","Yap/Taz","Medical Sciences","Medicine and Health Sciences","Neurosciences"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://dc.uthsc.edu/dissertations/105"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["<p>Normal brain development requires precise coordination of neural progenitor proliferation and differentiation, the mechanism of which is not well known. Recently the tumor suppressor neurofibromatosis 2 (Nf2) was shown to regulate the balance of neural progenitor proliferation and differentiation in the developing mouse brain through the Hippo pathway effectors, transcriptional coactivators Yap/Taz. The molecular mechanism of how Nf2 regulates Yap/Taz is not understood. Here I showed that Nf2 regulated the Yap/Taz activity by decreasing the stability of Yap/Taz. The regulation was independent of Yap-S366 phosphorylation, which is required for Yap degradation. I also showed that Nf2 did not regulate Lats1/2 kinases activity. Finally I found Nf2 interacted with Yap in mouse embryonic brain and identified the domains that were required for Nf2-Yap interaction. My study suggests that Nf2 may regulate Yap/Taz independent of the canonical Hippo pathway in the developing mammalian brain. </p>"]},{"key":"dc:title","label":"Title","values":["Preliminary Study on How Tumor Suppressor Nf2 Inhibits Transcriptional Coactivators Yap/Taz in the Developing Mouse Brain"]}]}],"canonical_facts":{"dc:contributor":["Xinwei Cao, Ph.D."],"dc:creator":["He, Yu"],"dc:date.available":["2016-06-07T07:00:00Z"],"dc:description.abstract":["<p>Normal brain development requires precise coordination of neural progenitor proliferation and differentiation, the mechanism of which is not well known. Recently the tumor suppressor neurofibromatosis 2 (Nf2) was shown to regulate the balance of neural progenitor proliferation and differentiation in the developing mouse brain through the Hippo pathway effectors, transcriptional coactivators Yap/Taz. The molecular mechanism of how Nf2 regulates Yap/Taz is not understood. Here I showed that Nf2 regulated the Yap/Taz activity by decreasing the stability of Yap/Taz. The regulation was independent of Yap-S366 phosphorylation, which is required for Yap degradation. I also showed that Nf2 did not regulate Lats1/2 kinases activity. Finally I found Nf2 interacted with Yap in mouse embryonic brain and identified the domains that were required for Nf2-Yap interaction. My study suggests that Nf2 may regulate Yap/Taz independent of the canonical Hippo pathway in the developing mammalian brain. </p>"],"dc:identifier":["https://dc.uthsc.edu/dissertations/105"],"dc:subject":["Brain development","Hippo signaling","Nf2/Merlin","Yap/Taz","Medical Sciences","Medicine and Health Sciences","Neurosciences"],"dc:title":["Preliminary Study on How Tumor Suppressor Nf2 Inhibits Transcriptional Coactivators Yap/Taz in the Developing Mouse Brain"],"thesis:degree_discipline":["Biomedical Sciences"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science (MS)"]},"updated_at":"2026-07-24T05:00:11Z"}