m(MIRBASE:"rno-mir-195")
Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667
Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667
Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667
Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
Endogenous miR-195 was knocked down using over-expression of its antisense molecule (pre-AMO-miR-195) via a lentivirus (lenti-pre-AMO-miR-195); this knockdown increased the tau phosphorylation at Ser202/Thr205, Ser262, Thr231, Ser422, and the Cdk5/p25 activation, but over-expression of miR-195 using lenti-pre-miR-195 decreased the tau phosphorylation and Cdk5/p25 activation. PubMed:26118667
A dual luciferase reporter assay showed that miR-195 bound to the Cdk5r1 gene, which encodes p35 protein, in the 3'UTR and inhibited p35 expression. PubMed:26118667
Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667
Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667
Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667
Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.