日誌
胃癌、肺癌引起乳癌？蛋白質降解有問題可能引起癌化？對抗癌症應該是依賴去磷酸化 ...
Hereditary diffuse gastric cancer (HDGC)
This condition is rare, but the lifetime stomach cancer risk among affected people is up to 70%. Women with this syndrome also have an increased risk of invasive lobular breast cancer. This syndrome is most often caused by mutations in the CDH1 gene.
遺傳性瀰漫性胃癌 (HDGC)
這種情況很少見，但受影響人群的終生胃癌風險高達 70%。 患有這種綜合徵的女性患浸潤性小葉乳腺癌的風險也會增加。 這種綜合徵最常由 CDH1 基因突變引起。
Breast cancer seems to be the most frequent metastatic cancer in the stomach (27.9%), followed by lung (23.8%), esophageal (19.1%)
乳腺癌似乎是胃部最常見的轉移癌 (27.9%)，其次是肺癌 (23.8%)、食道癌 (19.1%)
The Anaphase Promoting Complex or Cyclosome (APC/C) functions during mitosis to promote sister chromatid separation and mitotic exit through the degradation of mitotic cyclins and securin.
後期促進複合體或環狀體 (APC/C) 在有絲分裂期間發揮作用，通過降解有絲分裂細胞週期蛋白和 securin 促進姐妹染色單體分離和有絲分裂退出。
Once in G1 APC/C Cdh1 acts as a tumor suppressor and halts cells in a quiescent state.
一旦進入 G1，APC/C Cdh1 就會充當腫瘤抑制因子並使細胞停止處於靜止狀態。
The Anaphase Promoting Complex/Cyclosome (APC/C) ubiquitin ligase activated by its G1 specific adaptor protein Cdh1 is a major regulator of the cell cycle.
由其 G1 特異性銜接蛋白 Cdh1 激活的後期促進複合物/細胞週期體 (APC/C) 泛素連接酶是細胞週期的主要調節因子。
The APC/C Cdh1 mediates degradation of dozens of proteins
APC/C Cdh1 介導數十種蛋白質的降解
APC/C must be inactivated by phosphorylation of its cofactor, Cdh1.
APC/C 必須通過其輔助因子 Cdh1 的磷酸化而失活。
The APC/C is activated by two cofactors, Cdc20 and Cdh1.
APC/C 由兩個輔因子 Cdc20 和 Cdh1 激活。
When all the threonine residues are phosphorylated, Cdc20 binding to and activation of the APC/C are inhibited.
當所有蘇氨酸殘基都被磷酸化時，Cdc20 與 APC/C 的結合和激活就會受到抑制。
Dephosphorylation of Cdc20 is required for its C-box-dependent activation of the APC/C
Cdc20 的去磷酸化是 APC/C 的 C 盒依賴性激活所必需的
所以連同上述的Cdh1都需要去磷酸化激活
早衰老症或長相看起來很老，可能缺少基因蛋白的去磷酸化，去極化可激發去磷酸化。
告訴我們：
基因突變可能是缺少去磷酸化，導致蛋白質不穩定。
總結以上：
瀰漫性胃癌最常由 CDH1 基因突變引起+APC/C Cdh1 介導數十種蛋白質的降解+APC/C Cdh1充當腫瘤抑制因子
因此
如果蛋白質降解有問題
可能會引起癌症(癌化)
又
APC/C 由兩個輔因子 Cdc20 和 Cdh1 激活+Cdc20連同上述的Cdh1都需要去磷酸化激活+去極化可激發去磷酸化
所以
對抗癌症最主要應該是依賴去磷酸化
