磷酸變位 的英文怎麼說
中文拼音 [līnsuānbiànwèi]
磷酸變位
英文
phosphomutase-
In thl1 gene, there are some famililar enzyme digest sites including bamh i, hind, sac i and sal i. the sequence of thl1l from brassica oleracea l. shows 99 % identity to the sequence of thll from brassica napus l. there are some phosphorylation sites and an active site of thoiredoxin h members consisting of cppc in thll protein
甘藍和油菜thl1基因序列有5個堿基的差異，而氨基酸僅有2個氨基酸的變異，同源性達99 。在thl1蛋白的氨基酸序列中發現了一個硫氧還蛋白家族的活性位點（ cppc ）和多個磷酸化位點。Oocyte maturation involves the activation of various signal trans - duction pathways that converge to activate maturation - promoting factor ( mpf ) ; this is a key activity that catalyses entry into m - phase of meiosis i and meiosis ii
在爪蟾卵中有大量未被激活的cdc2 - cyclinb復合物，稱為pre - mpf ， pre - mpf在tyr15位脫磷酸變成活性mpf ，起到這個作用的磷酸酶是cdc25 ， cdc25的活性通過磷酸化和細胞位置進行調控。These results indicate that the alteration of cell proliferation and dna synthesis caused by different gnt - v cdna transfection may at least partly result from the modification of n - glycan structure and function of egfr. it seems that the increased 1, 6 glcnac branch on the n - glycans of egfr may benefit to its binding with egf and the resulting tyrosine auto - phosphorylatio n, while the decrease of this branch may prevent these processes
用特異性抗體結合westemblot結果發現，正義或反義gnt一vcdna的轉染並不引起pkb 、 p44 / 42mapk和mek蛋白質表達的變化，而gntv一s / h 」 21細胞pkbt308 、 5473位點磷酸化和免疫沉澱pkb的酪氨酸磷酸化以及以gsk召a /日磷酸化為指標的pkb的活性都較mock細胞增加， gntv一as / h7721細胞中這些指標的變化則相反。There is a relationship between catenin phosphorylation, translocation and tumoregenesis, further more, in this relationship, cell signaling cascade and mitogen and their receptors are involved. base on these evidences, people are trying to disturb the key molecules in this signaling cascade for anti - tumor purpose
表皮生長因子（ egf ）能使p120 ~ （ ctn ）酪氨酸磷酸化，磷酸化使bel - 7404細胞的粘附能力降低而遷移行為增強； p120 ~ （ ctn ）在細胞內的分佈出現明顯的核內轉位， -連環蛋白也出現相似的變化。Methods : in cultured lung explants without serum, the lipid component synthesis of pulmonary surfactant was evaluated in [ 3h ] - choline incorporation ; mrna content of phosphocholine cytidylyltransferase ( cct ) in lung explants was investigated in rt - pcr ; the changes of the ultrastructure of the at ii cells were observed with electron microscope ; the expression of nmdar1 subtype was observed in immunohistochemistry staining ; nitric oxide synthase ( nos ) activity, nitric oxide ( no ) content, superoxide dismutase ( sod ) level, malondialdehyde ( mda ) content and lactae dehydroase ( ldh ) level were determined by biochemistry methods. results : 1. influence of glutamate on synthesis of the lipid component of pulmonary surfactant ? with l - arginine, glu inhibited [ 3h ] - choline incorporation with good dose - dependence and time - dependence ; ( 2 ) mrna content of cct of the glu treatment groups was decreased ; ( 3 ) glu increases the release of ldh in cultured lung explants ; ( dwith electron microscope histochemistry, glu induced the changes of the ultrastruture of at ii iv cells
方法：採用成年大鼠肺組織無血清培養，運用[ ~ 3h ] -膽堿摻入法測定ps主要脂質磷脂酰膽堿（ pc ）合成量； rt - pcr擴增檢測肺組織中pc合成限速酶磷酸膽堿二胞苷酰基轉移酶（ cct ） mrna含量；透射電子顯微鏡法觀察肺泡型上皮細胞和ps系統超微結構的變化；免疫組織化學染色檢測glu的受體nmdar1亞單位的表達；生化測定肺組織乳酸脫氫酶（ ldh ）釋放量和肺組織勻漿中一氧化氮合酶（ nos ）活性、一氧化氮（ no ）生成量、超氧化物歧化酶（ sod ）水平以及丙二醛（ mda ）含量。To make clear the hypothesis, a middle cerebral artery occlusion ( mcao ) and hypoxia and glucose - deprivation ( hgd ) ischemic models were used in in vivo and in vitro study, respectively. we first studied the cellular localization of kvl. 2 and the co - localization of kvl. 2 protein and vegf receptors flk - 1 and flt - 1, observed the effect of mcao on kvl. 2 expression and phosphrylation in the rat brain in vivo, then investigated the effect of vegf on ischemia / hypoxia cell damage and tyrosine phosphorylation of kvl. 2 in sh - sy5y cells. finally, in order to further elucidate the relationship between vegf ' s neuroprotection and its regulation on kvl. 2 phosphorylation, we used a specific antisense oligodeoxynucleotide ( odn ) to knockdown the expression of endogenous vegf to observe its role in ischemia / hypoxia cell damage and regulation of kvl. 2 phosphorylation
為了驗證上述假設，本文分別在整體和離體水平，採用大腦中動脈缺血（ middlecerebralarteryocclusion ， mcao ）和體外氧?糖剝奪（ hypoxiaandglucose - deprivation ， hgd ）缺血模型，首先了解了kv1 . 2蛋白的細胞定位及與vegf受體flk - 1和flt - 1的共存情況，觀察了整體mcao后缺血再灌不同時間大鼠腦內kv1 . 2蛋白的磷酸化水平變化，然後通過外源性給予vegf蛋白，在sh - sy5y細胞株上觀察其對缺血細胞存活率及kv1 . 2蛋白磷酸化水平的影響，最後利用vegf反義脫氧寡核苷酸（ oligodeoxynucleotide ， odn ）特異阻斷內源性vegf蛋白的表達，觀察內源性vegf蛋白在缺血細胞損傷及調節kv1 . 2蛋白磷酸化中的作用，以進一步明確vegf缺血保護效應與其調節kv1 . 2蛋白磷酸化之間的關系。分享友人