In our work the conditioned avoidance training of Fyn deficient mice was carried out in a one way avoidance box.
提出了行为模型的选择对研究学习和记忆的重要性。
Objective To investigate whether the tyrosine protein kinase Src and Fyn were involved in the neuronal cell death induced by cerebral ischemia followed by reperfusion.
目的 观察胞内可溶性酪氨酸蛋白激酶Src、Fyn蛋白对脑缺血再灌注后海马CA1区神经细胞存活的影响。
Effects of chronic multiple stress on learning and memory and the expression of Fyn, BDNF, TrkB in the hippocampus of rats［J］.
慢性复合应激性学习记忆增强大鼠海马神经细胞增殖和突触后酪氨酸激酶表达的变化［J］。
Fyn Beijing law firm Ze-Min Tang, Hong-Yun Zhang believes that within the Green Area is directly related to people`s living quality.
菲英岛律师事务所北京泽敏唐，张红云认为，在绿化面积，直接关系到人民的生活质量。
A city of southern Denmark on Fyn Island near the Odense Fjord, an arm of the Kattegat.
欧登塞市在菲恩岛上，位于丹麦南部的城市，其附近的欧登塞湾是卡特加特海峡的一部。
Both Src and Fyn play an important role in neuronal death induced by cerebral ischemia followed by reperfusion, while Src dominate over Fyn in the process.
胞内可溶性酪氨酸蛋白激酶Src、Fyn蛋白的含量降低对脑缺血再灌注后海马神经细胞有明显保护作用，且以Src作用更为明显。
Objective To investigate whether tyrosine protein kinases Src and Fyn were involved in the phosphorylation of NR2A induced by cerebral ischemia followed by reperfusion. Methods Transient (15 min) brain ischemia was induced by the four-vessel occlusion in Sprague-Dawley rats. The antisense oligodeoxynucleotides of Src and Fyn were used to suppress the expression of Src and Fyn by intracerebroventricular infusion once a day for 3 days before ischemia.
近年来，最受人们关注的缺血性脑损伤机制是兴奋性氨基酸（excitatory amino acid，EAA）的神经毒性作用及神经元内钙超载触发的级联反应［1］，其中NMDA受体的NR2亚基在缺血性脑损伤中起着非常重要的作用，在缺血/再灌注（ischemia/ reperfusion，I/R）过程中其蛋白表达、磷酸化水平均有改变。
Results Both Src and Fyn antisense ODNs showed a protective role against neuronal cell death induced by cerebral ischemia/reperfusion. Furthermore, administration of Src antisense ODNs had more protective effect on the neuronal death than Fyn antisense ODNs.
结果 Src、Fyn反义寡核苷酸对脑缺血再灌注后海马CA1神经细胞均有明显保护作用，以Src AS ODNs保护作用更明显，与缺血组比较约有50%细胞存活(P.05)。
Western blot was used to examine the phosphorylation of NR2A in rat hippocampus. Results Both Src and Fyn antisense ODNs could decrease the phosphorylation of NR2A induced by cerebral ischemia/reperfusion, while administration of Src antisense ODNs had more suppressive effect on the phosphorylation of NR2A than Fyn antisense ODNs.
对NR2亚基有磷酸化调节作用的是Src家族酪氨酸蛋白激酶（Src family of protein tyrosine kinase，Src PTKs），这是一类膜结合的非受体酪氨酸蛋白激酶；现已知Src家族成员中Src、Fyn、Yes、Lyn、Lck在中枢神经系统中均有表达。
Methods Transient (15min) brain ischemia was induced by the four-vessel occlusion in Sprague Dawleyrats. The antisense oligodeoxynucleotides of Src and Fyn were used to suppress the expression of Src and Fyn by intracerebroventricular infusion once per day for 3 days before ischemia. After 5 days reperfusion, rats were perfusion-fixed with paraformaldehyde and cresyl violet staining were used to examine the survival of CA1 pyramidal cells of hippocampus.
采用Pulsinelli-Brierley 4动脉阻塞(4-VO)大鼠全脑缺血模型，缺血前连续3d脑室注射Src、Fyn反义寡核苷酸(antisense oligodeoxy-nucletides，AS ODNs)抑制Src、Fyn蛋白的表达后缺血，复灌5d，石蜡切片，焦油紫染色，图像分析测定单位面积内焦油紫染色细胞面积总和，与缺血组及错义寡核苷酸组(missense oligodeoxy-nucletides，MS ODNs)比较进行形态学分析。
Similar enrichment of IL-4 inducibility in peripheral NK1-CD4+CD8-CD44low T cells was observed in mice carrying disrupted p59fyn or il4r genes.
相似的结果也在剔除p59fyn或IL-4R基因的小鼠中发现。
Studies in neuropsychopharmacology and molecular neurobiology indicate that neurotransmitters and its receptors play important roles in alcohol abuse and addiction, and post-receptor signal transduction pathways, including cyclic adenosine 3', 5'-monophosphate-protein kinase A, phosphoinositide, Ca(superscript 2+)-calmodulin, phospholipase D and tyrosine kinase Fyn signaling cascade.
神经精神药理学和神经分子生物学研究表明，酒精滥用和成瘾不仅与中枢神经系统的神经递质及其相关的受体有关，而且，受体后的信号转导通路参与了酒精依赖的形成过程。其中包括环磷酸腺苷-蛋白激酶A、磷脂酰肌醇、Ca(上标 2+)-钙调蛋白、磷脂酶D以及酪氨酸激酶Fyn等信号途径。
The lack of Fyn in testis can lead to delayed formatio n of seminiferous tubule and degeneration of cells.
研究证明：Fyn蛋白存在于支持细胞的细胞骨架，Fyn缺损可导致生精小管形成延缓，并出现细胞变性。
On the basis of these results it may be concluded that Fyn deficiency impairs associative learning.
根据以上实验结果可以认为，Fyn-激酶缺损可导致小鼠的联合型学习能力下降。
However, no deficit of 2 week memory retention of homozygous Fyn kinase deficient mice was found.
然而，纯合子Fyn-激酶缺损小鼠的两周记忆保持与其他两组相比没有显著性差别。
These results suggest that Fyn may participate in the process of the enhanced learning and memory by chronic multiple stress.
提示Fyn参与了慢性复合性应激增强大鼠学习记忆能力的过程。
Proto-oncogene fyn protein tyrosine kinase (PTK) activity and its tyrosine phosphorylation were explored in granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor inducing growth signal transduction in murine macrophages.
本实验研究了小鼠巨噬细胞中原癌基因fyn酪氨酸蛋白激酶（PTK）的活性和酪氨酸磷酸化过程在粒-巨噬细胞集落刺激因子（GM-CSF）受体诱导的信号转导中的作用。
Proliferation and expression of hippocampal cells and change of postsynaptic density Fyn in the hippocampus of the rat whose learning and memory was enhanced by chronic multiple stress
慢性复合应激性学习记忆增强大鼠海马神经细胞增殖和突触后酪氨酸激酶表达的变化