缺氧诱导因子对基因表达的调控
中文名称
通路描述
HIF-alpha (HIF1A, HIF2A (EPAS1), HIF3A) 被转运至细胞核，可能通过两种途径：importin 4/7 (Chachami et al. 2009) 和 importin alpha/beta (Depping et al. 2008)。进入细胞核后，HIF-alpha 异二聚体与 HIF-beta (ARNT) 结合 (Wang et al. 1995, Jiang et al. 1996, Tian et al. 1997, Gu et al. 1998, Erbel et al. 2003)，并招募 CBP 和 p300 到靶基因的启动子区域 (Ebert and Bunn 1998, Kallio et al. 1998, Ema et al. 1999, Gu et al. 2001, Dames et al. 2002, Freedman et al. 2002)。
英文描述
Signaling by FGFR3 fusions in cancer In recent years, recurrent fusions of FGFR3 have been identified in a number of cancers, including glioblastoma and cancers of the lung and bladder, among others (Singh et al, 2012; Parker et al, 2013; Williams et al, 2013; Wu et al, 2013; Capelletti et al, 2014; Yuan et al, 2014; Wang et al, 2014; Carneiro et al, 2015; reviewed in Parker et al, 2014). The most common fusion partner of FGFR3 is TACC3 (transforming acidic coiled coil protein 3), a protein involved in mitotic spindle assembly and chromosome segregation (Lin et al, 2010; Burgess et al, 2015). FGFR3 fusions are constitutively active and may form oligomers in a ligand-independent manner based on dimerization domains provided by the fusion partner (Singh et al, 2012; Williams et al, 2013; Parker et al, 2013; reviewed in Parker et al, 2014). Transformation and proliferation appear to be promoted through activation of the ERK and AKT signaling pathways. In contrast, PLC gamma signaling is not stimulated downstream of FGFR3 fusions, as the PLC gamma docking site is not present in the fusion. FGFR3 fusions are sensitive to protein kinase inhibitors, suggesting their potential as therapeutic targets (Singh et al, 2012; Williams et al, 2013; Wu et al, 2013; reviewed in Parker et al, 2014).
所含基因
2 个基因