Ignet

Gene Information

Gene symbol: CDK5

Gene name: cyclin-dependent kinase 5

HGNC ID: 1774

Synonyms: PSSALRE

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	APLP2	1 hits
3	CDK5R1	1 hits
4	CDK5R2	1 hits
5	CDKAL1	1 hits
6	CREB1	1 hits
7	DES	1 hits
8	HHEX	1 hits
9	HIF1A	1 hits
10	HNF1A	1 hits
11	INS	1 hits
12	KCNQ1	1 hits
13	MAP3K14	1 hits
14	MAPK1	1 hits
15	MAPK3	1 hits
16	MAPK8	1 hits
17	MAPT	1 hits
18	MYC	1 hits
19	NES	1 hits
20	PDX1	1 hits
21	PPP1R1B	1 hits
22	SETD2	1 hits
23	SIRT1	1 hits
24	SYN1	1 hits
25	TCF7	1 hits
26	TCF7L2	1 hits
27	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	11443123	Cyclin-dependent kinase 5 promotes insulin exocytosis.
2	11443123	Recently it was shown that Cdk5 modulates dopamine signaling in neurons by regulating DARPP-32 function.
3	11443123	In addition, Cdk5 phosphorylates munc-18 and synapsin I, two essential components of the exocytotic machinery.
4	11443123	We have shown by reverse transcriptase-polymerase chain reaction, immunocytochemistry, and Western blotting that Cdk5 is present in the insulin-secreting pancreatic beta-cell.
5	11443123	Inhibition of Cdk5 with roscovitine reduced insulin secretion with approximately 35% compared with control after glucose stimulation and with approximately 65% after depolarization with glucose and KCl.
6	11443123	Taken together these results show that Cdk5 is present in beta-cells and acts as a positive regulator of insulin exocytosis.
7	11443123	Cyclin-dependent kinase 5 promotes insulin exocytosis.
8	11443123	Recently it was shown that Cdk5 modulates dopamine signaling in neurons by regulating DARPP-32 function.
9	11443123	In addition, Cdk5 phosphorylates munc-18 and synapsin I, two essential components of the exocytotic machinery.
10	11443123	We have shown by reverse transcriptase-polymerase chain reaction, immunocytochemistry, and Western blotting that Cdk5 is present in the insulin-secreting pancreatic beta-cell.
11	11443123	Inhibition of Cdk5 with roscovitine reduced insulin secretion with approximately 35% compared with control after glucose stimulation and with approximately 65% after depolarization with glucose and KCl.
12	11443123	Taken together these results show that Cdk5 is present in beta-cells and acts as a positive regulator of insulin exocytosis.
13	11443123	Cyclin-dependent kinase 5 promotes insulin exocytosis.
14	11443123	Recently it was shown that Cdk5 modulates dopamine signaling in neurons by regulating DARPP-32 function.
15	11443123	In addition, Cdk5 phosphorylates munc-18 and synapsin I, two essential components of the exocytotic machinery.
16	11443123	We have shown by reverse transcriptase-polymerase chain reaction, immunocytochemistry, and Western blotting that Cdk5 is present in the insulin-secreting pancreatic beta-cell.
17	11443123	Inhibition of Cdk5 with roscovitine reduced insulin secretion with approximately 35% compared with control after glucose stimulation and with approximately 65% after depolarization with glucose and KCl.
18	11443123	Taken together these results show that Cdk5 is present in beta-cells and acts as a positive regulator of insulin exocytosis.
19	11443123	Cyclin-dependent kinase 5 promotes insulin exocytosis.
20	11443123	Recently it was shown that Cdk5 modulates dopamine signaling in neurons by regulating DARPP-32 function.
21	11443123	In addition, Cdk5 phosphorylates munc-18 and synapsin I, two essential components of the exocytotic machinery.
22	11443123	We have shown by reverse transcriptase-polymerase chain reaction, immunocytochemistry, and Western blotting that Cdk5 is present in the insulin-secreting pancreatic beta-cell.
23	11443123	Inhibition of Cdk5 with roscovitine reduced insulin secretion with approximately 35% compared with control after glucose stimulation and with approximately 65% after depolarization with glucose and KCl.
24	11443123	Taken together these results show that Cdk5 is present in beta-cells and acts as a positive regulator of insulin exocytosis.
25	11443123	Cyclin-dependent kinase 5 promotes insulin exocytosis.
26	11443123	Recently it was shown that Cdk5 modulates dopamine signaling in neurons by regulating DARPP-32 function.
27	11443123	In addition, Cdk5 phosphorylates munc-18 and synapsin I, two essential components of the exocytotic machinery.
28	11443123	We have shown by reverse transcriptase-polymerase chain reaction, immunocytochemistry, and Western blotting that Cdk5 is present in the insulin-secreting pancreatic beta-cell.
29	11443123	Inhibition of Cdk5 with roscovitine reduced insulin secretion with approximately 35% compared with control after glucose stimulation and with approximately 65% after depolarization with glucose and KCl.
30	11443123	Taken together these results show that Cdk5 is present in beta-cells and acts as a positive regulator of insulin exocytosis.
31	11443123	Cyclin-dependent kinase 5 promotes insulin exocytosis.
32	11443123	Recently it was shown that Cdk5 modulates dopamine signaling in neurons by regulating DARPP-32 function.
33	11443123	In addition, Cdk5 phosphorylates munc-18 and synapsin I, two essential components of the exocytotic machinery.
34	11443123	We have shown by reverse transcriptase-polymerase chain reaction, immunocytochemistry, and Western blotting that Cdk5 is present in the insulin-secreting pancreatic beta-cell.
35	11443123	Inhibition of Cdk5 with roscovitine reduced insulin secretion with approximately 35% compared with control after glucose stimulation and with approximately 65% after depolarization with glucose and KCl.
36	11443123	Taken together these results show that Cdk5 is present in beta-cells and acts as a positive regulator of insulin exocytosis.
37	14976144	Glucose-induced expression of the cyclin-dependent protein kinase 5 activator p35 involved in Alzheimer's disease regulates insulin gene transcription in pancreatic beta-cells.
38	14976144	The deposition of amyloid within the insulin-producing islets of Langerhans in the pancreas is a common pathological finding in patients with type 2 diabetes.
39	14976144	Overactivity of CDK5 occurs by proteolytic cleavage and cellular mislocalization of its activator, p35.
40	14976144	These alterations in p35/CDK5 signaling pathway may mediate, at least in part, the functional abnormalities characteristic of Alzheimer's disease.
41	14976144	In this study we report that both the p35 and CDK5 genes are expressed in insulin-producing beta-cells of the pancreas.
42	14976144	We detect in beta-cells the formation of an active p35/CDK5 complex with specific kinase activity.
43	14976144	Notably, elevations of the extracellular concentration of glucose result in increases in p35 mRNA and protein levels that parallel elevations of p35/CDK5 activity.
44	14976144	Functional studies show that p35 stimulates the activity of the insulin promoter and that the stimulation requires CDK5 because stimulation is blocked by roscovitine, an inhibitor of CDK5 activity, a dominant negative form of CDK5, and small interfering RNAs against p35.
45	14976144	Our findings indicate that the expression of p35 and CDK5 in insulin-producing beta-cells ensembles a new signaling pathway, the activity of which is controlled by glucose, and its functional role may comprise the regulation of various biological processes in beta-cells, such as is the case for expression of the insulin gene.
46	14976144	Glucose-induced expression of the cyclin-dependent protein kinase 5 activator p35 involved in Alzheimer's disease regulates insulin gene transcription in pancreatic beta-cells.
47	14976144	The deposition of amyloid within the insulin-producing islets of Langerhans in the pancreas is a common pathological finding in patients with type 2 diabetes.
48	14976144	Overactivity of CDK5 occurs by proteolytic cleavage and cellular mislocalization of its activator, p35.
49	14976144	These alterations in p35/CDK5 signaling pathway may mediate, at least in part, the functional abnormalities characteristic of Alzheimer's disease.
50	14976144	In this study we report that both the p35 and CDK5 genes are expressed in insulin-producing beta-cells of the pancreas.
51	14976144	We detect in beta-cells the formation of an active p35/CDK5 complex with specific kinase activity.
52	14976144	Notably, elevations of the extracellular concentration of glucose result in increases in p35 mRNA and protein levels that parallel elevations of p35/CDK5 activity.
53	14976144	Functional studies show that p35 stimulates the activity of the insulin promoter and that the stimulation requires CDK5 because stimulation is blocked by roscovitine, an inhibitor of CDK5 activity, a dominant negative form of CDK5, and small interfering RNAs against p35.
54	14976144	Our findings indicate that the expression of p35 and CDK5 in insulin-producing beta-cells ensembles a new signaling pathway, the activity of which is controlled by glucose, and its functional role may comprise the regulation of various biological processes in beta-cells, such as is the case for expression of the insulin gene.
55	14976144	Glucose-induced expression of the cyclin-dependent protein kinase 5 activator p35 involved in Alzheimer's disease regulates insulin gene transcription in pancreatic beta-cells.
56	14976144	The deposition of amyloid within the insulin-producing islets of Langerhans in the pancreas is a common pathological finding in patients with type 2 diabetes.
57	14976144	Overactivity of CDK5 occurs by proteolytic cleavage and cellular mislocalization of its activator, p35.
58	14976144	These alterations in p35/CDK5 signaling pathway may mediate, at least in part, the functional abnormalities characteristic of Alzheimer's disease.
59	14976144	In this study we report that both the p35 and CDK5 genes are expressed in insulin-producing beta-cells of the pancreas.
60	14976144	We detect in beta-cells the formation of an active p35/CDK5 complex with specific kinase activity.
61	14976144	Notably, elevations of the extracellular concentration of glucose result in increases in p35 mRNA and protein levels that parallel elevations of p35/CDK5 activity.
62	14976144	Functional studies show that p35 stimulates the activity of the insulin promoter and that the stimulation requires CDK5 because stimulation is blocked by roscovitine, an inhibitor of CDK5 activity, a dominant negative form of CDK5, and small interfering RNAs against p35.
63	14976144	Our findings indicate that the expression of p35 and CDK5 in insulin-producing beta-cells ensembles a new signaling pathway, the activity of which is controlled by glucose, and its functional role may comprise the regulation of various biological processes in beta-cells, such as is the case for expression of the insulin gene.
64	14976144	Glucose-induced expression of the cyclin-dependent protein kinase 5 activator p35 involved in Alzheimer's disease regulates insulin gene transcription in pancreatic beta-cells.
65	14976144	The deposition of amyloid within the insulin-producing islets of Langerhans in the pancreas is a common pathological finding in patients with type 2 diabetes.
66	14976144	Overactivity of CDK5 occurs by proteolytic cleavage and cellular mislocalization of its activator, p35.
67	14976144	These alterations in p35/CDK5 signaling pathway may mediate, at least in part, the functional abnormalities characteristic of Alzheimer's disease.
68	14976144	In this study we report that both the p35 and CDK5 genes are expressed in insulin-producing beta-cells of the pancreas.
69	14976144	We detect in beta-cells the formation of an active p35/CDK5 complex with specific kinase activity.
70	14976144	Notably, elevations of the extracellular concentration of glucose result in increases in p35 mRNA and protein levels that parallel elevations of p35/CDK5 activity.
71	14976144	Functional studies show that p35 stimulates the activity of the insulin promoter and that the stimulation requires CDK5 because stimulation is blocked by roscovitine, an inhibitor of CDK5 activity, a dominant negative form of CDK5, and small interfering RNAs against p35.
72	14976144	Our findings indicate that the expression of p35 and CDK5 in insulin-producing beta-cells ensembles a new signaling pathway, the activity of which is controlled by glucose, and its functional role may comprise the regulation of various biological processes in beta-cells, such as is the case for expression of the insulin gene.
73	14976144	Glucose-induced expression of the cyclin-dependent protein kinase 5 activator p35 involved in Alzheimer's disease regulates insulin gene transcription in pancreatic beta-cells.
74	14976144	The deposition of amyloid within the insulin-producing islets of Langerhans in the pancreas is a common pathological finding in patients with type 2 diabetes.
75	14976144	Overactivity of CDK5 occurs by proteolytic cleavage and cellular mislocalization of its activator, p35.
76	14976144	These alterations in p35/CDK5 signaling pathway may mediate, at least in part, the functional abnormalities characteristic of Alzheimer's disease.
77	14976144	In this study we report that both the p35 and CDK5 genes are expressed in insulin-producing beta-cells of the pancreas.
78	14976144	We detect in beta-cells the formation of an active p35/CDK5 complex with specific kinase activity.
79	14976144	Notably, elevations of the extracellular concentration of glucose result in increases in p35 mRNA and protein levels that parallel elevations of p35/CDK5 activity.
80	14976144	Functional studies show that p35 stimulates the activity of the insulin promoter and that the stimulation requires CDK5 because stimulation is blocked by roscovitine, an inhibitor of CDK5 activity, a dominant negative form of CDK5, and small interfering RNAs against p35.
81	14976144	Our findings indicate that the expression of p35 and CDK5 in insulin-producing beta-cells ensembles a new signaling pathway, the activity of which is controlled by glucose, and its functional role may comprise the regulation of various biological processes in beta-cells, such as is the case for expression of the insulin gene.
82	14976144	Glucose-induced expression of the cyclin-dependent protein kinase 5 activator p35 involved in Alzheimer's disease regulates insulin gene transcription in pancreatic beta-cells.
83	14976144	The deposition of amyloid within the insulin-producing islets of Langerhans in the pancreas is a common pathological finding in patients with type 2 diabetes.
84	14976144	Overactivity of CDK5 occurs by proteolytic cleavage and cellular mislocalization of its activator, p35.
85	14976144	These alterations in p35/CDK5 signaling pathway may mediate, at least in part, the functional abnormalities characteristic of Alzheimer's disease.
86	14976144	In this study we report that both the p35 and CDK5 genes are expressed in insulin-producing beta-cells of the pancreas.
87	14976144	We detect in beta-cells the formation of an active p35/CDK5 complex with specific kinase activity.
88	14976144	Notably, elevations of the extracellular concentration of glucose result in increases in p35 mRNA and protein levels that parallel elevations of p35/CDK5 activity.
89	14976144	Functional studies show that p35 stimulates the activity of the insulin promoter and that the stimulation requires CDK5 because stimulation is blocked by roscovitine, an inhibitor of CDK5 activity, a dominant negative form of CDK5, and small interfering RNAs against p35.
90	14976144	Our findings indicate that the expression of p35 and CDK5 in insulin-producing beta-cells ensembles a new signaling pathway, the activity of which is controlled by glucose, and its functional role may comprise the regulation of various biological processes in beta-cells, such as is the case for expression of the insulin gene.
91	14976144	Glucose-induced expression of the cyclin-dependent protein kinase 5 activator p35 involved in Alzheimer's disease regulates insulin gene transcription in pancreatic beta-cells.
92	14976144	The deposition of amyloid within the insulin-producing islets of Langerhans in the pancreas is a common pathological finding in patients with type 2 diabetes.
93	14976144	Overactivity of CDK5 occurs by proteolytic cleavage and cellular mislocalization of its activator, p35.
94	14976144	These alterations in p35/CDK5 signaling pathway may mediate, at least in part, the functional abnormalities characteristic of Alzheimer's disease.
95	14976144	In this study we report that both the p35 and CDK5 genes are expressed in insulin-producing beta-cells of the pancreas.
96	14976144	We detect in beta-cells the formation of an active p35/CDK5 complex with specific kinase activity.
97	14976144	Notably, elevations of the extracellular concentration of glucose result in increases in p35 mRNA and protein levels that parallel elevations of p35/CDK5 activity.
98	14976144	Functional studies show that p35 stimulates the activity of the insulin promoter and that the stimulation requires CDK5 because stimulation is blocked by roscovitine, an inhibitor of CDK5 activity, a dominant negative form of CDK5, and small interfering RNAs against p35.
99	14976144	Our findings indicate that the expression of p35 and CDK5 in insulin-producing beta-cells ensembles a new signaling pathway, the activity of which is controlled by glucose, and its functional role may comprise the regulation of various biological processes in beta-cells, such as is the case for expression of the insulin gene.
100	15908038	Cyclin-dependent kinase 5 activators p35 and p39 facilitate formation of functional synapses.
101	15908038	Cdk5 needs to associate with one of the regulatory proteins p35 or p39 to be an active enzyme.
102	15908038	To investigate if Cdk5 plays a role in the establishment of functional synapses, we have characterized the expression of Cdk5, p35, and p39 in the neuroblastoma-glioma cell line NG108-15, and recorded postsynaptic activity in myotubes in response to presynaptic overexpression of Cdk5, p35, and p39.
103	15908038	Endogenous Cdk5 and p35 protein levels increased with cellular differentiation and preferentially distributed to soluble pools, whereas the level of p39 protein remained low and primarily was present in membrane and cytoskeletal fractions.
104	15908038	Overexpression of either Cdk5/p35 or Cdk5/p39 resulted in a substantial increase in synaptic structures that displayed postsynaptic activities, as well as mEPP frequency.
105	15908038	These findings demonstrate that Cdk5, p35, and p39 are endogenously expressed in NG108-15 cells, exhibit distinct subcellular localizations, and that both Cdk5/p35 and Cdk5/p39 are central in formation of functional synapses.
106	15908038	Cyclin-dependent kinase 5 activators p35 and p39 facilitate formation of functional synapses.
107	15908038	Cdk5 needs to associate with one of the regulatory proteins p35 or p39 to be an active enzyme.
108	15908038	To investigate if Cdk5 plays a role in the establishment of functional synapses, we have characterized the expression of Cdk5, p35, and p39 in the neuroblastoma-glioma cell line NG108-15, and recorded postsynaptic activity in myotubes in response to presynaptic overexpression of Cdk5, p35, and p39.
109	15908038	Endogenous Cdk5 and p35 protein levels increased with cellular differentiation and preferentially distributed to soluble pools, whereas the level of p39 protein remained low and primarily was present in membrane and cytoskeletal fractions.
110	15908038	Overexpression of either Cdk5/p35 or Cdk5/p39 resulted in a substantial increase in synaptic structures that displayed postsynaptic activities, as well as mEPP frequency.
111	15908038	These findings demonstrate that Cdk5, p35, and p39 are endogenously expressed in NG108-15 cells, exhibit distinct subcellular localizations, and that both Cdk5/p35 and Cdk5/p39 are central in formation of functional synapses.
112	15908038	Cyclin-dependent kinase 5 activators p35 and p39 facilitate formation of functional synapses.
113	15908038	Cdk5 needs to associate with one of the regulatory proteins p35 or p39 to be an active enzyme.
114	15908038	To investigate if Cdk5 plays a role in the establishment of functional synapses, we have characterized the expression of Cdk5, p35, and p39 in the neuroblastoma-glioma cell line NG108-15, and recorded postsynaptic activity in myotubes in response to presynaptic overexpression of Cdk5, p35, and p39.
115	15908038	Endogenous Cdk5 and p35 protein levels increased with cellular differentiation and preferentially distributed to soluble pools, whereas the level of p39 protein remained low and primarily was present in membrane and cytoskeletal fractions.
116	15908038	Overexpression of either Cdk5/p35 or Cdk5/p39 resulted in a substantial increase in synaptic structures that displayed postsynaptic activities, as well as mEPP frequency.
117	15908038	These findings demonstrate that Cdk5, p35, and p39 are endogenously expressed in NG108-15 cells, exhibit distinct subcellular localizations, and that both Cdk5/p35 and Cdk5/p39 are central in formation of functional synapses.
118	15908038	Cyclin-dependent kinase 5 activators p35 and p39 facilitate formation of functional synapses.
119	15908038	Cdk5 needs to associate with one of the regulatory proteins p35 or p39 to be an active enzyme.
120	15908038	To investigate if Cdk5 plays a role in the establishment of functional synapses, we have characterized the expression of Cdk5, p35, and p39 in the neuroblastoma-glioma cell line NG108-15, and recorded postsynaptic activity in myotubes in response to presynaptic overexpression of Cdk5, p35, and p39.
121	15908038	Endogenous Cdk5 and p35 protein levels increased with cellular differentiation and preferentially distributed to soluble pools, whereas the level of p39 protein remained low and primarily was present in membrane and cytoskeletal fractions.
122	15908038	Overexpression of either Cdk5/p35 or Cdk5/p39 resulted in a substantial increase in synaptic structures that displayed postsynaptic activities, as well as mEPP frequency.
123	15908038	These findings demonstrate that Cdk5, p35, and p39 are endogenously expressed in NG108-15 cells, exhibit distinct subcellular localizations, and that both Cdk5/p35 and Cdk5/p39 are central in formation of functional synapses.
124	15908038	Cyclin-dependent kinase 5 activators p35 and p39 facilitate formation of functional synapses.
125	15908038	Cdk5 needs to associate with one of the regulatory proteins p35 or p39 to be an active enzyme.
126	15908038	To investigate if Cdk5 plays a role in the establishment of functional synapses, we have characterized the expression of Cdk5, p35, and p39 in the neuroblastoma-glioma cell line NG108-15, and recorded postsynaptic activity in myotubes in response to presynaptic overexpression of Cdk5, p35, and p39.
127	15908038	Endogenous Cdk5 and p35 protein levels increased with cellular differentiation and preferentially distributed to soluble pools, whereas the level of p39 protein remained low and primarily was present in membrane and cytoskeletal fractions.
128	15908038	Overexpression of either Cdk5/p35 or Cdk5/p39 resulted in a substantial increase in synaptic structures that displayed postsynaptic activities, as well as mEPP frequency.
129	15908038	These findings demonstrate that Cdk5, p35, and p39 are endogenously expressed in NG108-15 cells, exhibit distinct subcellular localizations, and that both Cdk5/p35 and Cdk5/p39 are central in formation of functional synapses.
130	15908038	Cyclin-dependent kinase 5 activators p35 and p39 facilitate formation of functional synapses.
131	15908038	Cdk5 needs to associate with one of the regulatory proteins p35 or p39 to be an active enzyme.
132	15908038	To investigate if Cdk5 plays a role in the establishment of functional synapses, we have characterized the expression of Cdk5, p35, and p39 in the neuroblastoma-glioma cell line NG108-15, and recorded postsynaptic activity in myotubes in response to presynaptic overexpression of Cdk5, p35, and p39.
133	15908038	Endogenous Cdk5 and p35 protein levels increased with cellular differentiation and preferentially distributed to soluble pools, whereas the level of p39 protein remained low and primarily was present in membrane and cytoskeletal fractions.
134	15908038	Overexpression of either Cdk5/p35 or Cdk5/p39 resulted in a substantial increase in synaptic structures that displayed postsynaptic activities, as well as mEPP frequency.
135	15908038	These findings demonstrate that Cdk5, p35, and p39 are endogenously expressed in NG108-15 cells, exhibit distinct subcellular localizations, and that both Cdk5/p35 and Cdk5/p39 are central in formation of functional synapses.
136	16155576	Here we show that inhibition of the activity of cyclin-dependent kinase 5 (Cdk5) enhanced insulin secretion under conditions of stimulation by high glucose but not low glucose in MIN6 cells and pancreatic islets.
137	16155576	The role of Cdk5 in regulation of insulin secretion was confirmed in pancreatic beta cells deficient in p35, an activator of Cdk5. p35-knockout mice also showed enhanced insulin secretion in response to a glucose challenge.
138	16155576	These results suggest that Cdk5/p35 may be a drug target for the regulation of glucose-stimulated insulin secretion.
139	16155576	Here we show that inhibition of the activity of cyclin-dependent kinase 5 (Cdk5) enhanced insulin secretion under conditions of stimulation by high glucose but not low glucose in MIN6 cells and pancreatic islets.
140	16155576	The role of Cdk5 in regulation of insulin secretion was confirmed in pancreatic beta cells deficient in p35, an activator of Cdk5. p35-knockout mice also showed enhanced insulin secretion in response to a glucose challenge.
141	16155576	These results suggest that Cdk5/p35 may be a drug target for the regulation of glucose-stimulated insulin secretion.
142	16155576	Here we show that inhibition of the activity of cyclin-dependent kinase 5 (Cdk5) enhanced insulin secretion under conditions of stimulation by high glucose but not low glucose in MIN6 cells and pancreatic islets.
143	16155576	The role of Cdk5 in regulation of insulin secretion was confirmed in pancreatic beta cells deficient in p35, an activator of Cdk5. p35-knockout mice also showed enhanced insulin secretion in response to a glucose challenge.
144	16155576	These results suggest that Cdk5/p35 may be a drug target for the regulation of glucose-stimulated insulin secretion.
145	16887799	Neuronal dysfunction in Alzheimer patients has been linked to overactivity of the cyclin-dependent kinase 5 (CDK5) and its activator p35.
146	16887799	Further, glucose enhances p35 gene expression, promoting the formation of active p35/CDK5 complexes that regulate the expression of the insulin gene.
147	16887799	We therefore postulated that CDK5 and p35 may be responsible for this beta cell impairment and that inhibition of CDK5 might have a beneficial effect.
148	16887799	Inhibition of CDK5 prevented this decrease of insulin gene expression.
149	16887799	We used DNA binding (gel shift) assays and Western immunoblots to demonstrate that cellular levels of the transcription factor PDX-1, normally decreased by glucotoxicity, were preserved with CDK5 inhibition, as was the binding of PDX-1 to the insulin promoter.
150	16887799	Analyses of nuclear and cytoplasmic PDX-1 protein levels revealed that CDK5 inhibition restores nuclear PDX-1, without affecting its cytoplasmic concentration, suggesting that CDK5 regulates the nuclear/cytoplasm partitioning of PDX-1.
151	16887799	Using a Myc-tagged PDX-1 construct, we showed that the translocation of PDX-1 from the nucleus to the cytoplasm during glucotoxic conditions was prevented when CDK5 was inhibited.
152	16887799	Neuronal dysfunction in Alzheimer patients has been linked to overactivity of the cyclin-dependent kinase 5 (CDK5) and its activator p35.
153	16887799	Further, glucose enhances p35 gene expression, promoting the formation of active p35/CDK5 complexes that regulate the expression of the insulin gene.
154	16887799	We therefore postulated that CDK5 and p35 may be responsible for this beta cell impairment and that inhibition of CDK5 might have a beneficial effect.
155	16887799	Inhibition of CDK5 prevented this decrease of insulin gene expression.
156	16887799	We used DNA binding (gel shift) assays and Western immunoblots to demonstrate that cellular levels of the transcription factor PDX-1, normally decreased by glucotoxicity, were preserved with CDK5 inhibition, as was the binding of PDX-1 to the insulin promoter.
157	16887799	Analyses of nuclear and cytoplasmic PDX-1 protein levels revealed that CDK5 inhibition restores nuclear PDX-1, without affecting its cytoplasmic concentration, suggesting that CDK5 regulates the nuclear/cytoplasm partitioning of PDX-1.
158	16887799	Using a Myc-tagged PDX-1 construct, we showed that the translocation of PDX-1 from the nucleus to the cytoplasm during glucotoxic conditions was prevented when CDK5 was inhibited.
159	16887799	Neuronal dysfunction in Alzheimer patients has been linked to overactivity of the cyclin-dependent kinase 5 (CDK5) and its activator p35.
160	16887799	Further, glucose enhances p35 gene expression, promoting the formation of active p35/CDK5 complexes that regulate the expression of the insulin gene.
161	16887799	We therefore postulated that CDK5 and p35 may be responsible for this beta cell impairment and that inhibition of CDK5 might have a beneficial effect.
162	16887799	Inhibition of CDK5 prevented this decrease of insulin gene expression.
163	16887799	We used DNA binding (gel shift) assays and Western immunoblots to demonstrate that cellular levels of the transcription factor PDX-1, normally decreased by glucotoxicity, were preserved with CDK5 inhibition, as was the binding of PDX-1 to the insulin promoter.
164	16887799	Analyses of nuclear and cytoplasmic PDX-1 protein levels revealed that CDK5 inhibition restores nuclear PDX-1, without affecting its cytoplasmic concentration, suggesting that CDK5 regulates the nuclear/cytoplasm partitioning of PDX-1.
165	16887799	Using a Myc-tagged PDX-1 construct, we showed that the translocation of PDX-1 from the nucleus to the cytoplasm during glucotoxic conditions was prevented when CDK5 was inhibited.
166	16887799	Neuronal dysfunction in Alzheimer patients has been linked to overactivity of the cyclin-dependent kinase 5 (CDK5) and its activator p35.
167	16887799	Further, glucose enhances p35 gene expression, promoting the formation of active p35/CDK5 complexes that regulate the expression of the insulin gene.
168	16887799	We therefore postulated that CDK5 and p35 may be responsible for this beta cell impairment and that inhibition of CDK5 might have a beneficial effect.
169	16887799	Inhibition of CDK5 prevented this decrease of insulin gene expression.
170	16887799	We used DNA binding (gel shift) assays and Western immunoblots to demonstrate that cellular levels of the transcription factor PDX-1, normally decreased by glucotoxicity, were preserved with CDK5 inhibition, as was the binding of PDX-1 to the insulin promoter.
171	16887799	Analyses of nuclear and cytoplasmic PDX-1 protein levels revealed that CDK5 inhibition restores nuclear PDX-1, without affecting its cytoplasmic concentration, suggesting that CDK5 regulates the nuclear/cytoplasm partitioning of PDX-1.
172	16887799	Using a Myc-tagged PDX-1 construct, we showed that the translocation of PDX-1 from the nucleus to the cytoplasm during glucotoxic conditions was prevented when CDK5 was inhibited.
173	16887799	Neuronal dysfunction in Alzheimer patients has been linked to overactivity of the cyclin-dependent kinase 5 (CDK5) and its activator p35.
174	16887799	Further, glucose enhances p35 gene expression, promoting the formation of active p35/CDK5 complexes that regulate the expression of the insulin gene.
175	16887799	We therefore postulated that CDK5 and p35 may be responsible for this beta cell impairment and that inhibition of CDK5 might have a beneficial effect.
176	16887799	Inhibition of CDK5 prevented this decrease of insulin gene expression.
177	16887799	We used DNA binding (gel shift) assays and Western immunoblots to demonstrate that cellular levels of the transcription factor PDX-1, normally decreased by glucotoxicity, were preserved with CDK5 inhibition, as was the binding of PDX-1 to the insulin promoter.
178	16887799	Analyses of nuclear and cytoplasmic PDX-1 protein levels revealed that CDK5 inhibition restores nuclear PDX-1, without affecting its cytoplasmic concentration, suggesting that CDK5 regulates the nuclear/cytoplasm partitioning of PDX-1.
179	16887799	Using a Myc-tagged PDX-1 construct, we showed that the translocation of PDX-1 from the nucleus to the cytoplasm during glucotoxic conditions was prevented when CDK5 was inhibited.
180	16887799	Neuronal dysfunction in Alzheimer patients has been linked to overactivity of the cyclin-dependent kinase 5 (CDK5) and its activator p35.
181	16887799	Further, glucose enhances p35 gene expression, promoting the formation of active p35/CDK5 complexes that regulate the expression of the insulin gene.
182	16887799	We therefore postulated that CDK5 and p35 may be responsible for this beta cell impairment and that inhibition of CDK5 might have a beneficial effect.
183	16887799	Inhibition of CDK5 prevented this decrease of insulin gene expression.
184	16887799	We used DNA binding (gel shift) assays and Western immunoblots to demonstrate that cellular levels of the transcription factor PDX-1, normally decreased by glucotoxicity, were preserved with CDK5 inhibition, as was the binding of PDX-1 to the insulin promoter.
185	16887799	Analyses of nuclear and cytoplasmic PDX-1 protein levels revealed that CDK5 inhibition restores nuclear PDX-1, without affecting its cytoplasmic concentration, suggesting that CDK5 regulates the nuclear/cytoplasm partitioning of PDX-1.
186	16887799	Using a Myc-tagged PDX-1 construct, we showed that the translocation of PDX-1 from the nucleus to the cytoplasm during glucotoxic conditions was prevented when CDK5 was inhibited.
187	16887799	Neuronal dysfunction in Alzheimer patients has been linked to overactivity of the cyclin-dependent kinase 5 (CDK5) and its activator p35.
188	16887799	Further, glucose enhances p35 gene expression, promoting the formation of active p35/CDK5 complexes that regulate the expression of the insulin gene.
189	16887799	We therefore postulated that CDK5 and p35 may be responsible for this beta cell impairment and that inhibition of CDK5 might have a beneficial effect.
190	16887799	Inhibition of CDK5 prevented this decrease of insulin gene expression.
191	16887799	We used DNA binding (gel shift) assays and Western immunoblots to demonstrate that cellular levels of the transcription factor PDX-1, normally decreased by glucotoxicity, were preserved with CDK5 inhibition, as was the binding of PDX-1 to the insulin promoter.
192	16887799	Analyses of nuclear and cytoplasmic PDX-1 protein levels revealed that CDK5 inhibition restores nuclear PDX-1, without affecting its cytoplasmic concentration, suggesting that CDK5 regulates the nuclear/cytoplasm partitioning of PDX-1.
193	16887799	Using a Myc-tagged PDX-1 construct, we showed that the translocation of PDX-1 from the nucleus to the cytoplasm during glucotoxic conditions was prevented when CDK5 was inhibited.
194	17979810	Cyclin-dependent kinase 5 (Cdk5) is a serine/threonine protein kinase, which forms active complexes with p35 or p39 expressed predominantly in neurons.
195	17979810	It has been widely accepted that aberrant Cdk5 activity induced by the conversion of p35 to p25 plays roles in the pathogenesis of neurodegenerative diseases.
196	17979810	Moreover, recent studies suggest that Cdk5 plays crucial roles in physiological functions in non-neuronal cells such as glucose-stimulated insulin secretion in pancreatic -cells.
197	17979810	This review focuses on the implication of Cdk5 in the signaling pathways of both neurodegenerative diseases and drug abuse, and the mechanism of Cdk5 involvement in insulin secretion.
198	17979810	Cyclin-dependent kinase 5 (Cdk5) is a serine/threonine protein kinase, which forms active complexes with p35 or p39 expressed predominantly in neurons.
199	17979810	It has been widely accepted that aberrant Cdk5 activity induced by the conversion of p35 to p25 plays roles in the pathogenesis of neurodegenerative diseases.
200	17979810	Moreover, recent studies suggest that Cdk5 plays crucial roles in physiological functions in non-neuronal cells such as glucose-stimulated insulin secretion in pancreatic -cells.
201	17979810	This review focuses on the implication of Cdk5 in the signaling pathways of both neurodegenerative diseases and drug abuse, and the mechanism of Cdk5 involvement in insulin secretion.
202	17979810	Cyclin-dependent kinase 5 (Cdk5) is a serine/threonine protein kinase, which forms active complexes with p35 or p39 expressed predominantly in neurons.
203	17979810	It has been widely accepted that aberrant Cdk5 activity induced by the conversion of p35 to p25 plays roles in the pathogenesis of neurodegenerative diseases.
204	17979810	Moreover, recent studies suggest that Cdk5 plays crucial roles in physiological functions in non-neuronal cells such as glucose-stimulated insulin secretion in pancreatic -cells.
205	17979810	This review focuses on the implication of Cdk5 in the signaling pathways of both neurodegenerative diseases and drug abuse, and the mechanism of Cdk5 involvement in insulin secretion.
206	17979810	Cyclin-dependent kinase 5 (Cdk5) is a serine/threonine protein kinase, which forms active complexes with p35 or p39 expressed predominantly in neurons.
207	17979810	It has been widely accepted that aberrant Cdk5 activity induced by the conversion of p35 to p25 plays roles in the pathogenesis of neurodegenerative diseases.
208	17979810	Moreover, recent studies suggest that Cdk5 plays crucial roles in physiological functions in non-neuronal cells such as glucose-stimulated insulin secretion in pancreatic -cells.
209	17979810	This review focuses on the implication of Cdk5 in the signaling pathways of both neurodegenerative diseases and drug abuse, and the mechanism of Cdk5 involvement in insulin secretion.
210	19461118	Furthermore, both statins reduced expression of microtubule-associated protein tau in astrocytes (P < 0.01), while both statins increased its expression in neuroblastoma cells (P < 0.01).
211	19461118	In SK-N-SH cells, simvastatin significantly increased cyclin-dependent kinase 5 and glycogen synthase kinase 3beta expression, while pravastatin increased amyloid precursor protein expression.
212	19718565	Genetic variants of cyclin-dependent kinase 5 regulatory subunit associated protein 1-like 1 and transcription factor 7-like 2 are not associated with polycystic ovary syndrome in Chinese women.
213	19718565	Novel risk loci for type 2 diabetes, single nucleotide polymorphism (SNP) rs7756992 in cyclin-dependent kinase 5 (CDK5) regulatory subunit associated protein 1-like 1 (CDKAL1), rs290487 and rs11196218 in transcription factor 7-like 2 (TCF7L2), were recently identified.
214	19718565	We concluded that rs7756992 in CDKAL1, rs290487 and rs11196218 in TCF7L2 have no associations with PCOS or PCOS-related clinical features.
215	19718565	Genetic variants of cyclin-dependent kinase 5 regulatory subunit associated protein 1-like 1 and transcription factor 7-like 2 are not associated with polycystic ovary syndrome in Chinese women.
216	19718565	Novel risk loci for type 2 diabetes, single nucleotide polymorphism (SNP) rs7756992 in cyclin-dependent kinase 5 (CDK5) regulatory subunit associated protein 1-like 1 (CDKAL1), rs290487 and rs11196218 in transcription factor 7-like 2 (TCF7L2), were recently identified.
217	19718565	We concluded that rs7756992 in CDKAL1, rs290487 and rs11196218 in TCF7L2 have no associations with PCOS or PCOS-related clinical features.
218	19763399	This review discusses current evidence on the contribution of oxygen deprivation to AD, with an emphasis on hypoxia inducible transcription factor-1 (HIF-1)-mediated pathways and the association of AD with the cytoskeleton regulator cyclin-dependent kinase 5.
219	21368910	Heterogeneity of genetic associations of CDKAL1 and HHEX with susceptibility of type 2 diabetes mellitus by gender.
220	21368910	One was located near the gene of hematopoietically expressed homeobox (HHEX), and the others were all in the gene of cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like 1 (CDKAL1).
221	21368910	Further analysis revealed that the sequence variant (rs5015480) near HHEX and two SNPs (rs7756992 and rs9465871) in CDKAL1 were associated with the susceptibility of T2DM in females (P<0.005), but not in males (P>0.005).
222	21368910	We suggested heterogeneous genetic associations of the T2DM susceptibility with the CDKAL1 and HHEX genes by gender.
223	21611789	On chromosome 6q22.3, a cluster of single-nucleotide polymorphisms located in intron 5 of the cyclin-dependent kinase 5 (CDK5) regulatory subunit-associated protein 1-like 1 (CDKAL1) gene were shown to confer susceptibility to type 2 diabetes in multiple ethnic groups.
224	21611789	The diabetogenic role of CDKAL1 variants is suggested to consist in lower insulin secretion probably due to the insufficient inhibition of the CDK5 activity.
225	21611789	On chromosome 6q22.3, a cluster of single-nucleotide polymorphisms located in intron 5 of the cyclin-dependent kinase 5 (CDK5) regulatory subunit-associated protein 1-like 1 (CDKAL1) gene were shown to confer susceptibility to type 2 diabetes in multiple ethnic groups.
226	21611789	The diabetogenic role of CDKAL1 variants is suggested to consist in lower insulin secretion probably due to the insufficient inhibition of the CDK5 activity.
227	21841312	With regard to genetic factors, variations in the gene encoding Cdk5 regulatory associated protein 1-like 1 (Cdkal1) have been associated with an impaired insulin response and increased risk of T2D across different ethnic populations, but the molecular function of this protein has not been characterized.
228	21841312	Here, we show that Cdkal1 is a mammalian methylthiotransferase that biosynthesizes 2-methylthio-N6-threonylcarbamoyladenosine (ms2t6A) in tRNA(Lys)(UUU) and that it is required for the accurate translation of AAA and AAG codons.
229	21841312	Mice with pancreatic β cell-specific KO of Cdkal1 (referred to herein as β cell KO mice) showed pancreatic islet hypertrophy, a decrease in insulin secretion, and impaired blood glucose control.
230	22028710	Cyclin-Dependent Kinase 5/p35/p39: A Novel and Imminent Therapeutic Target for Diabetes Mellitus.
231	22028710	Present therapies to minify hyperglycaemia and insulin resistance mainly target ATP-sensitive K(+) channels (K(ATP)) of pancreatic cells and PPAR-γ to enhance the insulin secretion and potential for GLUT expression, respectively.
232	22028710	CDK5 is a serine/threonine protein kinase, which forms active complexes with p35 or p39 found principally in neurons and in pancreatic β cells.
233	22028710	Pieces of evidence from recent studies recommend the vital role of CDK5 in physiological functions in nonneuronal cells such as glucose-stimulated insulin secretion in pancreatic cells.
234	22028710	Inhibition of CDK5 averts the decrease of insulin gene expression through the inhibition of nuclear translocation of PDX-1 which is a transcription factor for the insulin gene.
235	22028710	The present pieces of evidence designate that CDK5 might be a potential drug target for the regulation of glucose-stimulated insulin secretion in the treatment of diabetes mellitus.
236	22028710	Cyclin-Dependent Kinase 5/p35/p39: A Novel and Imminent Therapeutic Target for Diabetes Mellitus.
237	22028710	Present therapies to minify hyperglycaemia and insulin resistance mainly target ATP-sensitive K(+) channels (K(ATP)) of pancreatic cells and PPAR-γ to enhance the insulin secretion and potential for GLUT expression, respectively.
238	22028710	CDK5 is a serine/threonine protein kinase, which forms active complexes with p35 or p39 found principally in neurons and in pancreatic β cells.
239	22028710	Pieces of evidence from recent studies recommend the vital role of CDK5 in physiological functions in nonneuronal cells such as glucose-stimulated insulin secretion in pancreatic cells.
240	22028710	Inhibition of CDK5 averts the decrease of insulin gene expression through the inhibition of nuclear translocation of PDX-1 which is a transcription factor for the insulin gene.
241	22028710	The present pieces of evidence designate that CDK5 might be a potential drug target for the regulation of glucose-stimulated insulin secretion in the treatment of diabetes mellitus.
242	22028710	Cyclin-Dependent Kinase 5/p35/p39: A Novel and Imminent Therapeutic Target for Diabetes Mellitus.
243	22028710	Present therapies to minify hyperglycaemia and insulin resistance mainly target ATP-sensitive K(+) channels (K(ATP)) of pancreatic cells and PPAR-γ to enhance the insulin secretion and potential for GLUT expression, respectively.
244	22028710	CDK5 is a serine/threonine protein kinase, which forms active complexes with p35 or p39 found principally in neurons and in pancreatic β cells.
245	22028710	Pieces of evidence from recent studies recommend the vital role of CDK5 in physiological functions in nonneuronal cells such as glucose-stimulated insulin secretion in pancreatic cells.
246	22028710	Inhibition of CDK5 averts the decrease of insulin gene expression through the inhibition of nuclear translocation of PDX-1 which is a transcription factor for the insulin gene.
247	22028710	The present pieces of evidence designate that CDK5 might be a potential drug target for the regulation of glucose-stimulated insulin secretion in the treatment of diabetes mellitus.
248	22028710	Cyclin-Dependent Kinase 5/p35/p39: A Novel and Imminent Therapeutic Target for Diabetes Mellitus.
249	22028710	Present therapies to minify hyperglycaemia and insulin resistance mainly target ATP-sensitive K(+) channels (K(ATP)) of pancreatic cells and PPAR-γ to enhance the insulin secretion and potential for GLUT expression, respectively.
250	22028710	CDK5 is a serine/threonine protein kinase, which forms active complexes with p35 or p39 found principally in neurons and in pancreatic β cells.
251	22028710	Pieces of evidence from recent studies recommend the vital role of CDK5 in physiological functions in nonneuronal cells such as glucose-stimulated insulin secretion in pancreatic cells.
252	22028710	Inhibition of CDK5 averts the decrease of insulin gene expression through the inhibition of nuclear translocation of PDX-1 which is a transcription factor for the insulin gene.
253	22028710	The present pieces of evidence designate that CDK5 might be a potential drug target for the regulation of glucose-stimulated insulin secretion in the treatment of diabetes mellitus.
254	22028710	Cyclin-Dependent Kinase 5/p35/p39: A Novel and Imminent Therapeutic Target for Diabetes Mellitus.
255	22028710	Present therapies to minify hyperglycaemia and insulin resistance mainly target ATP-sensitive K(+) channels (K(ATP)) of pancreatic cells and PPAR-γ to enhance the insulin secretion and potential for GLUT expression, respectively.
256	22028710	CDK5 is a serine/threonine protein kinase, which forms active complexes with p35 or p39 found principally in neurons and in pancreatic β cells.
257	22028710	Pieces of evidence from recent studies recommend the vital role of CDK5 in physiological functions in nonneuronal cells such as glucose-stimulated insulin secretion in pancreatic cells.
258	22028710	Inhibition of CDK5 averts the decrease of insulin gene expression through the inhibition of nuclear translocation of PDX-1 which is a transcription factor for the insulin gene.
259	22028710	The present pieces of evidence designate that CDK5 might be a potential drug target for the regulation of glucose-stimulated insulin secretion in the treatment of diabetes mellitus.
260	22290723	Association of glycosylated hemoglobin with the gene encoding CDKAL1 in the Korean Association Resource (KARE) study.
261	22290723	We first identified sequence variants within a linkage disequilibrium block (r(2) > 0.98) in the intron 5 of cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like 1 (CDKAL1) gene using 4,275 normoglycemic subjects of Cohort 1 (P < 2.5 × 10(-8)).
262	22290723	Especially, a strong association with 1 h glucose (P = 1.3 × 10(-11)) led us to interpreting that CDKAL1 might influence the level of glycosylated hemoglobin by affecting 1 h glucose level.
263	22290723	Ultimately, accumulated effects on the glycosylated hemoglobin level by the genetic variation of CDKAL1 might affect susceptibility to type 2 diabetes mellitus.
264	22427718	Histone deacetylase (HDAC) inhibitor is emphasized as a new class of insulin sensitizer here.
265	22427718	Regulators of SIRT1, CREB, NO, p38, ERK and Cdk5 are discussed in the activation of PPARγ.
266	22437209	We used TaqMan OpenArray and Sequenom MassARRAY to genotype the four SNPs (rs4712523, rs7756992, rs4712524 and rs6931514) in CDKAL1 (cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like 1) at 6p22.3 and one SNP (rs9472138) near vascular endothelial growth factor A (VEGFA) at 6p21.1.
267	22437209	Our findings indicated that genetic variants of CDKAL1 and VEGFA on chromosome 6 may contribute to T2D risk in Chinese population, especially for rs9472138 at 6p21.1 identified for the first time to significantly increase the T2D risk in Chinese individuals.
268	22521314	Aim of the present study was to analyze the influence of obesity-associated hyperinsulinemia on tau phosphorylation without changes in glucose homeostasis. 15% high fat diet fed over 12-16 weeks induced 2.4-fold increased plasma insulin levels without changing glucose tolerance.
269	22521314	Additionally, chronic hyperinsulinemia did not influence downstream insulin receptor signaling and the expression of the tau kinases (e.g.
270	22521314	ERK-1/-2, Akt, GSK-3β, CDK5 or JNK) and tau phosphatases (e.g.
271	22521314	Thus, we successfully induced hyperinsulinemia without causing glucose intolerance in our experimental animals but this did not influence central insulin receptor signaling or tau phosphorylation.
272	22649490	Thiazolidinediones (TZDs) act through peroxisome proliferator activated receptor (PPAR) γ to increase insulin sensitivity in type 2 diabetes (T2DM), but deleterious effects of these ligands mean that selective modulators with improved clinical profiles are needed.
273	22649490	We verified that MCFAs (C8-C10) bind the PPARγ LBD in vitro and showed that they are low-potency partial agonists that display assay-specific actions relative to TZDs; they act as very weak partial agonists in transfections with PPARγ LBD, stronger partial agonists with full length PPARγ and exhibit full blockade of PPARγ phosphorylation by cyclin-dependent kinase 5 (cdk5), linked to reversal of adipose tissue insulin resistance.
274	22795893	Also atypical is the activation of Cdk5 by binding of a non-cyclin activator protein, namely, the Cdk5 regulatory proteins Cdk5R1 (p35), truncated Cdk5R1 (p25), or Cdk5R2 (p39).
275	22795893	Recently, this concept of a canonical neuronal function of Cdk5 has been extended, if not challenged, by the observation of p35 and p39 expression, as well as Cdk5 activity, in multiple non-neuronal cells.
276	22795893	Extraneuronal Cdk5 regulates critical biological processes including transcript-selective translation control for regulation of macrophage gene expression, glucose-inducible insulin secretion, hematopoietic cell differentiation, vascular angiogenesis, cell migration, senescence, and wound-healing, among others.
277	22795893	Also atypical is the activation of Cdk5 by binding of a non-cyclin activator protein, namely, the Cdk5 regulatory proteins Cdk5R1 (p35), truncated Cdk5R1 (p25), or Cdk5R2 (p39).
278	22795893	Recently, this concept of a canonical neuronal function of Cdk5 has been extended, if not challenged, by the observation of p35 and p39 expression, as well as Cdk5 activity, in multiple non-neuronal cells.
279	22795893	Extraneuronal Cdk5 regulates critical biological processes including transcript-selective translation control for regulation of macrophage gene expression, glucose-inducible insulin secretion, hematopoietic cell differentiation, vascular angiogenesis, cell migration, senescence, and wound-healing, among others.
280	22795893	Also atypical is the activation of Cdk5 by binding of a non-cyclin activator protein, namely, the Cdk5 regulatory proteins Cdk5R1 (p35), truncated Cdk5R1 (p25), or Cdk5R2 (p39).
281	22795893	Recently, this concept of a canonical neuronal function of Cdk5 has been extended, if not challenged, by the observation of p35 and p39 expression, as well as Cdk5 activity, in multiple non-neuronal cells.
282	22795893	Extraneuronal Cdk5 regulates critical biological processes including transcript-selective translation control for regulation of macrophage gene expression, glucose-inducible insulin secretion, hematopoietic cell differentiation, vascular angiogenesis, cell migration, senescence, and wound-healing, among others.
283	22891507	Results from current association studies on T2DM susceptible genes in GDM have shown significant heterogeneity There may be primary evidence that polymorphisms of susceptible genes of T2DM such as transcription factor 7-like 2 (TCF7L2) gene, potassium channel voltage-gate KQT-like subfamily member 1 (KCNQ1) gene, and cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like 1 (CDKAL1) gene, may increase risk of GDM.
284	23000950	The expression of intermediate filament protein nestin and its association with cyclin-dependent kinase 5 in the glomeruli of rats with diabetic nephropathy.
285	23581463	Troglitazone, a thiazolidinedione, decreases tau phosphorylation through the inhibition of cyclin-dependent kinase 5 activity in SH-SY5Y neuroblastoma cells and primary neurons.
286	23581463	Here, we investigated whether and how troglitazone, a parent TZD drug, inhibits tau phosphorylation.Treatment with troglitazone decreased tau-Thr231 phosphorylation and p35, the specific activator of cyclin-dependent kinase 5 (CDK5), in a dose- and time-dependent manner.
287	23581463	Troglitazone also decreased CDK5 enzymatic activity, and ectopic expression of p25, the cleaved and more active form of p35, restored the troglitazone-induced decrease in tau-Thr231 phosphorylation.
288	23581463	Treatment with various inhibitors revealed that troglitazone-induced inhibitions of tau-Thr231 phosphorylation and p35 expression were not mediated by glycogen synthase kinase 3b, protein kinase A, and protein phosphatase 2A signaling pathways.Finally, we also found that the same observed inhibitory effects of troglitazone hold true for the use of primary cortical neurons.
289	23581463	Taken together, we demonstrated that TZDs repressed tau-Thr231 phosphorylation via the inhibition of CDK5 activity, which was mediated by the proteasomal degradation of p35 and a PPARc-independent signaling pathway.
290	23581463	Troglitazone, a thiazolidinedione, decreases tau phosphorylation through the inhibition of cyclin-dependent kinase 5 activity in SH-SY5Y neuroblastoma cells and primary neurons.
291	23581463	Here, we investigated whether and how troglitazone, a parent TZD drug, inhibits tau phosphorylation.Treatment with troglitazone decreased tau-Thr231 phosphorylation and p35, the specific activator of cyclin-dependent kinase 5 (CDK5), in a dose- and time-dependent manner.
292	23581463	Troglitazone also decreased CDK5 enzymatic activity, and ectopic expression of p25, the cleaved and more active form of p35, restored the troglitazone-induced decrease in tau-Thr231 phosphorylation.
293	23581463	Treatment with various inhibitors revealed that troglitazone-induced inhibitions of tau-Thr231 phosphorylation and p35 expression were not mediated by glycogen synthase kinase 3b, protein kinase A, and protein phosphatase 2A signaling pathways.Finally, we also found that the same observed inhibitory effects of troglitazone hold true for the use of primary cortical neurons.
294	23581463	Taken together, we demonstrated that TZDs repressed tau-Thr231 phosphorylation via the inhibition of CDK5 activity, which was mediated by the proteasomal degradation of p35 and a PPARc-independent signaling pathway.
295	23581463	Troglitazone, a thiazolidinedione, decreases tau phosphorylation through the inhibition of cyclin-dependent kinase 5 activity in SH-SY5Y neuroblastoma cells and primary neurons.
296	23581463	Here, we investigated whether and how troglitazone, a parent TZD drug, inhibits tau phosphorylation.Treatment with troglitazone decreased tau-Thr231 phosphorylation and p35, the specific activator of cyclin-dependent kinase 5 (CDK5), in a dose- and time-dependent manner.
297	23581463	Troglitazone also decreased CDK5 enzymatic activity, and ectopic expression of p25, the cleaved and more active form of p35, restored the troglitazone-induced decrease in tau-Thr231 phosphorylation.
298	23581463	Treatment with various inhibitors revealed that troglitazone-induced inhibitions of tau-Thr231 phosphorylation and p35 expression were not mediated by glycogen synthase kinase 3b, protein kinase A, and protein phosphatase 2A signaling pathways.Finally, we also found that the same observed inhibitory effects of troglitazone hold true for the use of primary cortical neurons.
299	23581463	Taken together, we demonstrated that TZDs repressed tau-Thr231 phosphorylation via the inhibition of CDK5 activity, which was mediated by the proteasomal degradation of p35 and a PPARc-independent signaling pathway.
300	23581463	Troglitazone, a thiazolidinedione, decreases tau phosphorylation through the inhibition of cyclin-dependent kinase 5 activity in SH-SY5Y neuroblastoma cells and primary neurons.
301	23581463	Here, we investigated whether and how troglitazone, a parent TZD drug, inhibits tau phosphorylation.Treatment with troglitazone decreased tau-Thr231 phosphorylation and p35, the specific activator of cyclin-dependent kinase 5 (CDK5), in a dose- and time-dependent manner.
302	23581463	Troglitazone also decreased CDK5 enzymatic activity, and ectopic expression of p25, the cleaved and more active form of p35, restored the troglitazone-induced decrease in tau-Thr231 phosphorylation.
303	23581463	Treatment with various inhibitors revealed that troglitazone-induced inhibitions of tau-Thr231 phosphorylation and p35 expression were not mediated by glycogen synthase kinase 3b, protein kinase A, and protein phosphatase 2A signaling pathways.Finally, we also found that the same observed inhibitory effects of troglitazone hold true for the use of primary cortical neurons.
304	23581463	Taken together, we demonstrated that TZDs repressed tau-Thr231 phosphorylation via the inhibition of CDK5 activity, which was mediated by the proteasomal degradation of p35 and a PPARc-independent signaling pathway.