Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST. Alternatively we drive c-FOS to induce BST. In these various experimentally-induced model of BST, we analyze chromatin accessibility profiles upon Ras/MAPK activation and/or TGFb signaling abrogation. We also analyze chromatin accessibility profiles upon c-FOS activation.
Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST. Alternatively we drive c-FOS to induce BST. Here, we analyze transcriptional profiles upon c-FOS induction.
Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST. Alternatively we drive c-FOS to induce BST. Here, we analyze transcriptional profiles upon Ras/MAPK activation and/or TGFb signaling abrogation.
Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST. Alternatively we drive c-FOS to induce BST. Here, we analyze chromatin accessibility profiles upon c-FOS activation
Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST and examine the DNA binding profile of the AP-1 transcription factor c-FOS.
Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that either modulation of Ras/MAPK or TGFb signaling or c-FOS induction could drive BST. Enhanced EGFR signaling has been implicated during BST. Here, we analyze transcriptional profiles upon c-FOS induction when cells are treated with EGFR signaling inhibitors afatinib (5uM) and UO126 (10uM).
Project description:We sought to understand the change in the global gene expression profile of the ΔYGP1 strain in comparison with the BGL-6_Kl parental strain. The transcriptome analysis revealed the change in expression of genes involved in cell wall structure, biogenesis, and integrity that might contribute to the improvement of the BGL display efficiency phenotype.
Project description:To solve the problem of low FK520 production by Streptomyces hygroscopicus var. ascomyceticus FS35, PHB synthesis gene phaC and PHB decomposition gene fkbU were co-overexpressed in parent strain FS35 to construct recombinant strain OphaCfkbU. Surprisingly, recombinant strain OphaCfkbU accumulated more biomass than parent strain FS35 in whole fermentation. Therefore, to explore the effect of co-overexpression on the strain growth, comparative transcriptome analysis were carried out between parent strain FS35 and recombinant strain OphaCfkbU. Transcriptome data showed that co-overexpression increased the utilization of sugar sources and stimulated the generation of coenzymes, ribosome, acyl carrier proteins and sulfate donors. This study revealed the internal mechanism of the effect of PHB on strain growth, proving a reference for the role of PHB in other microorganisms.