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[求助]
求細胞免疫相關的大神翻譯3小段和肝再生細胞通路有關的話(已被精簡)
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1.Foxm1b在肝細胞再生G1/S相表達顯著增強, Foxm1b對細胞增殖的影響主要通過調控Skp2和Cks1編碼Skp-Cullin1-F-box(SCF)泛素連接酶復合物的亞基, 靶向作用于CDK抑制蛋白P21CIP1/WAF1、p27Kip在G1/S相轉換中降解, 進而影響某些Cyclin或Cdk活化劑Cdc25a、Cdc25b磷酸酶的活性, 同時他又能激活JNK1,共同調控G1/S的轉變. Foxm1b還參與生長激素(growth hormone, GH)介導的細胞增殖. 2.TGR5可于Kupffer細胞表面表達, 活化后可誘導細胞內胞內環(huán)磷腺苷(cyclic adenosine monophosphate,cAMP)升高, 可通過激活TGR5-cAMP途徑改善Kupffer細胞免疫功能, 抑制其產生過量的炎癥細胞因子而影響肝再生. 3.MAPKs是一類絲氨酸/蘇氨酸蛋白激酶, 可調節(jié)細胞增殖、凋亡等反應. MAPKs主要包括ERK、c-Jun氨基末端激酶(c-Jun NH2-terminal kinase, JNK)和p38MAPK通路,其中JNK和p38MAKP被稱為應激活化蛋白激酶,. 有研究顯示, 低濃度膽酸可使肝細胞JNK蛋白顯著上調, 而高濃度的膽酸則使p38MAPK蛋白表達顯著上調, 提示不同濃度的膽汁酸對肝再生的不同作用可能是通過調節(jié)JNK和p38MAKP途徑實現的. |
木蟲 (正式寫手)
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1.Foxm1b in regeneration G1 / S phase was significantly enhanced, Foxm1b mainly impacts on cell proliferation by regulating Skp2 and Cks1 in coding complex subunits of Skp-Cullin1-F-box (SCF) ubiquitin and ligase , targeting at the CDK to inhibit degradation of protein P21CIP1/WAF1, p27Kip in G1 / S phase conversion, thereby affecting activity certain Cyclin or Cdk activator Cdc25a, Cdc25b phosphatase, and he can activate JNK1, jointly regulate the transition of G1 / S. Foxm1b is also involved in process of the growth hormone (growth hormone, GH) mediating cell proliferation. 2.TGR5 can express on the surface of Kupffer cells , and after activation it can induce cell intracellular cyclic adenosine monophosphate (cyclic adenosine monophosphate, cAMP) to increase, by activating TGR5-cAMP pathway to improve the immune function of Kupffer cells to inhibit inflammatory cells to produce excessive factors affecting liver regeneration. 3.MAPKs are a class of serine / threonine protein kinase that regulates cell proliferation, apoptosis and other reactions. MAPKs mainly includ ERK, c-Jun N-terminal kinase (c-Jun NH2-terminal kinase, JNK) and p38MAPK pathway, among which JNK and p38MAKP are called stress-activated protein kinase. Studies have shown that low concentrations of acid can make JNK in liver cells increase significantly , while the high concentration of acid make the expression of p38MAPK protein significantly increase, suggesting that different concentrations of bile acids may effect on liver regeneration differently by regulating JNK and p38MAKP. 能力有限,僅供參考 |

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