![]() ![]() Dev Biol 433(1):94–107Ĭhuang JC, Raymond PA (2002) Embryonic origin of the eyes in teleost fish. Exp Eye Res 111:9–16īushnell HL et al (2018) JNK is antagonized to ensure the correct number of interommatidial cells pattern the Drosophila retina. Comput Struct Biotechnol J 15:307–319īeby F, Lamonerie T (2013) The homeobox gene Otx2 in development and disease. Development 121(10):3279–3290Īudagnotto M, Dal Peraro M (2017) Protein post-translational modifications: in silico prediction tools and molecular modeling. ConclusionĬ-Jun N-terminal kinase 1 (JNK1) phosphorylates OTX2 transcription factor through the protein–protein interaction.Īcampora D et al (1995) Forebrain and midbrain regions are deleted in Otx2-/-mutants due to a defective anterior neuroectoderm specification during gastrulation. In addition, we confirmed that the inactivation of JNK1 K55N mutant significantly reduced the JNK1-mediated phosphorylation of OTX2 by performing an immune complex protein kinase assay. The protein–protein interaction and co-localization between JNK1 and OTX2 were further validated in the developing P0 mouse retina. JNK1 directly interacted with OTX2 through the transactivation domain at the c-terminal region. In vivo and in vitro kinase assay of JNK1 was performed to detect the phosphorylation of OTX2 by JNK1. The protein interaction between JNK1 and OTX2 was identified with the co-immunoprecipitation and immunocytochemistry. To identify the binding partner of OTX2, we performed co-immunoprecipitation and detected with a pooled antibody that targeted effective kinases. The identification of JNK1 as an OTX2 regulatory protein through the protein interaction and phosphorylation. However, the regulatory mechanisms of OTX2 are poorly identified. The transcription factor orthodenticle homeobox 2 (OTX2) has critical functions in brain and eye development, and its mutations in humans are related to retinal diseases, such as ocular coloboma and microphthalmia. ![]()
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