Ignet

Gene Information

Gene symbol: CKM

Gene name: creatine kinase, muscle

HGNC ID: 1994

Related Genes

#	Gene Symbol	Number of hits
1	CKB	1 hits
2	CKMT1B	1 hits
3	CKMT2	1 hits
4	IGF1	1 hits
5	INS	1 hits
6	LPL	1 hits
7	MGEA5	1 hits
8	MYH14	1 hits
9	PPP2R4	1 hits

Related Sentences

#	PMID	Sentence
1	1387697	The effect of physical training on total creatine kinase (CK), CK-MM, and CK-MB isoenzyme activity was studied in hearts of diabetic and control rats.
2	1514612	Creatine kinase (CK) is important for energy transfer and is composed of mitochondrial (mitCK), muscle (MCK), and brain (BCK) subunits, each being the product of separate nuclear genes.
3	1514612	The concentrations of MCK and BCK mRNAs have been shown to decrease in streptozotocin-hypoinsulinemic rat hearts, and in this report, we examined in detail the diabetic effect on CK gene expression in cardiac muscle and in two types of skeletal muscle.
4	1514612	Creatine kinase (CK) is important for energy transfer and is composed of mitochondrial (mitCK), muscle (MCK), and brain (BCK) subunits, each being the product of separate nuclear genes.
5	1514612	The concentrations of MCK and BCK mRNAs have been shown to decrease in streptozotocin-hypoinsulinemic rat hearts, and in this report, we examined in detail the diabetic effect on CK gene expression in cardiac muscle and in two types of skeletal muscle.
6	1887884	Insulin responsiveness of CK-M and CK-B mRNA in the diabetic rat heart.
7	1887884	Recently, we found that creatine kinase (CK) enzyme activity and CK-M subunit mRNA levels are decreased in the heart of rats with experimental diabetes mellitus.
8	1887884	The CK-M and CK-B genes are expressed in the heart, and we wanted to determine whether diabetes also induces a change in CK-B mRNA levels.
9	1887884	Quantitation of CK-M and CK-B mRNA levels on Northern blots with specific cDNA probes showed that, in diabetic hearts, CK-B mRNA levels represent only 19.8% of control levels and are more markedly depressed than CK-M mRNA levels, which are 46.5% of control values.
10	1887884	Acute injection of insulin led to a significant 1.6-fold increase in CK-M mRNA and a 2.2-fold increase of CK-B mRNA 5 h after insulin injection.
11	1887884	CK-M mRNA levels were restored to normal within 12 h, but 48 h were required to restore CK-B mRNA levels to normal values.
12	1887884	After 1 mo of insulin therapy, CK-B mRNA levels had risen 9.7-fold, exceeding normal values by 90%, whereas CK-M mRNA levels were at the normal level as previously shown.
13	1887884	Diabetes leads therefore to a marked lowering of CK-M and CK-B mRNA levels in the rat heart.
14	1887884	Insulin responsiveness of CK-M and CK-B mRNA in the diabetic rat heart.
15	1887884	Recently, we found that creatine kinase (CK) enzyme activity and CK-M subunit mRNA levels are decreased in the heart of rats with experimental diabetes mellitus.
16	1887884	The CK-M and CK-B genes are expressed in the heart, and we wanted to determine whether diabetes also induces a change in CK-B mRNA levels.
17	1887884	Quantitation of CK-M and CK-B mRNA levels on Northern blots with specific cDNA probes showed that, in diabetic hearts, CK-B mRNA levels represent only 19.8% of control levels and are more markedly depressed than CK-M mRNA levels, which are 46.5% of control values.
18	1887884	Acute injection of insulin led to a significant 1.6-fold increase in CK-M mRNA and a 2.2-fold increase of CK-B mRNA 5 h after insulin injection.
19	1887884	CK-M mRNA levels were restored to normal within 12 h, but 48 h were required to restore CK-B mRNA levels to normal values.
20	1887884	After 1 mo of insulin therapy, CK-B mRNA levels had risen 9.7-fold, exceeding normal values by 90%, whereas CK-M mRNA levels were at the normal level as previously shown.
21	1887884	Diabetes leads therefore to a marked lowering of CK-M and CK-B mRNA levels in the rat heart.
22	1887884	Insulin responsiveness of CK-M and CK-B mRNA in the diabetic rat heart.
23	1887884	Recently, we found that creatine kinase (CK) enzyme activity and CK-M subunit mRNA levels are decreased in the heart of rats with experimental diabetes mellitus.
24	1887884	The CK-M and CK-B genes are expressed in the heart, and we wanted to determine whether diabetes also induces a change in CK-B mRNA levels.
25	1887884	Quantitation of CK-M and CK-B mRNA levels on Northern blots with specific cDNA probes showed that, in diabetic hearts, CK-B mRNA levels represent only 19.8% of control levels and are more markedly depressed than CK-M mRNA levels, which are 46.5% of control values.
26	1887884	Acute injection of insulin led to a significant 1.6-fold increase in CK-M mRNA and a 2.2-fold increase of CK-B mRNA 5 h after insulin injection.
27	1887884	CK-M mRNA levels were restored to normal within 12 h, but 48 h were required to restore CK-B mRNA levels to normal values.
28	1887884	After 1 mo of insulin therapy, CK-B mRNA levels had risen 9.7-fold, exceeding normal values by 90%, whereas CK-M mRNA levels were at the normal level as previously shown.
29	1887884	Diabetes leads therefore to a marked lowering of CK-M and CK-B mRNA levels in the rat heart.
30	1887884	Insulin responsiveness of CK-M and CK-B mRNA in the diabetic rat heart.
31	1887884	Recently, we found that creatine kinase (CK) enzyme activity and CK-M subunit mRNA levels are decreased in the heart of rats with experimental diabetes mellitus.
32	1887884	The CK-M and CK-B genes are expressed in the heart, and we wanted to determine whether diabetes also induces a change in CK-B mRNA levels.
33	1887884	Quantitation of CK-M and CK-B mRNA levels on Northern blots with specific cDNA probes showed that, in diabetic hearts, CK-B mRNA levels represent only 19.8% of control levels and are more markedly depressed than CK-M mRNA levels, which are 46.5% of control values.
34	1887884	Acute injection of insulin led to a significant 1.6-fold increase in CK-M mRNA and a 2.2-fold increase of CK-B mRNA 5 h after insulin injection.
35	1887884	CK-M mRNA levels were restored to normal within 12 h, but 48 h were required to restore CK-B mRNA levels to normal values.
36	1887884	After 1 mo of insulin therapy, CK-B mRNA levels had risen 9.7-fold, exceeding normal values by 90%, whereas CK-M mRNA levels were at the normal level as previously shown.
37	1887884	Diabetes leads therefore to a marked lowering of CK-M and CK-B mRNA levels in the rat heart.
38	1887884	Insulin responsiveness of CK-M and CK-B mRNA in the diabetic rat heart.
39	1887884	Recently, we found that creatine kinase (CK) enzyme activity and CK-M subunit mRNA levels are decreased in the heart of rats with experimental diabetes mellitus.
40	1887884	The CK-M and CK-B genes are expressed in the heart, and we wanted to determine whether diabetes also induces a change in CK-B mRNA levels.
41	1887884	Quantitation of CK-M and CK-B mRNA levels on Northern blots with specific cDNA probes showed that, in diabetic hearts, CK-B mRNA levels represent only 19.8% of control levels and are more markedly depressed than CK-M mRNA levels, which are 46.5% of control values.
42	1887884	Acute injection of insulin led to a significant 1.6-fold increase in CK-M mRNA and a 2.2-fold increase of CK-B mRNA 5 h after insulin injection.
43	1887884	CK-M mRNA levels were restored to normal within 12 h, but 48 h were required to restore CK-B mRNA levels to normal values.
44	1887884	After 1 mo of insulin therapy, CK-B mRNA levels had risen 9.7-fold, exceeding normal values by 90%, whereas CK-M mRNA levels were at the normal level as previously shown.
45	1887884	Diabetes leads therefore to a marked lowering of CK-M and CK-B mRNA levels in the rat heart.
46	1887884	Insulin responsiveness of CK-M and CK-B mRNA in the diabetic rat heart.
47	1887884	Recently, we found that creatine kinase (CK) enzyme activity and CK-M subunit mRNA levels are decreased in the heart of rats with experimental diabetes mellitus.
48	1887884	The CK-M and CK-B genes are expressed in the heart, and we wanted to determine whether diabetes also induces a change in CK-B mRNA levels.
49	1887884	Quantitation of CK-M and CK-B mRNA levels on Northern blots with specific cDNA probes showed that, in diabetic hearts, CK-B mRNA levels represent only 19.8% of control levels and are more markedly depressed than CK-M mRNA levels, which are 46.5% of control values.
50	1887884	Acute injection of insulin led to a significant 1.6-fold increase in CK-M mRNA and a 2.2-fold increase of CK-B mRNA 5 h after insulin injection.
51	1887884	CK-M mRNA levels were restored to normal within 12 h, but 48 h were required to restore CK-B mRNA levels to normal values.
52	1887884	After 1 mo of insulin therapy, CK-B mRNA levels had risen 9.7-fold, exceeding normal values by 90%, whereas CK-M mRNA levels were at the normal level as previously shown.
53	1887884	Diabetes leads therefore to a marked lowering of CK-M and CK-B mRNA levels in the rat heart.
54	1887884	Insulin responsiveness of CK-M and CK-B mRNA in the diabetic rat heart.
55	1887884	Recently, we found that creatine kinase (CK) enzyme activity and CK-M subunit mRNA levels are decreased in the heart of rats with experimental diabetes mellitus.
56	1887884	The CK-M and CK-B genes are expressed in the heart, and we wanted to determine whether diabetes also induces a change in CK-B mRNA levels.
57	1887884	Quantitation of CK-M and CK-B mRNA levels on Northern blots with specific cDNA probes showed that, in diabetic hearts, CK-B mRNA levels represent only 19.8% of control levels and are more markedly depressed than CK-M mRNA levels, which are 46.5% of control values.
58	1887884	Acute injection of insulin led to a significant 1.6-fold increase in CK-M mRNA and a 2.2-fold increase of CK-B mRNA 5 h after insulin injection.
59	1887884	CK-M mRNA levels were restored to normal within 12 h, but 48 h were required to restore CK-B mRNA levels to normal values.
60	1887884	After 1 mo of insulin therapy, CK-B mRNA levels had risen 9.7-fold, exceeding normal values by 90%, whereas CK-M mRNA levels were at the normal level as previously shown.
61	1887884	Diabetes leads therefore to a marked lowering of CK-M and CK-B mRNA levels in the rat heart.
62	1887884	Insulin responsiveness of CK-M and CK-B mRNA in the diabetic rat heart.
63	1887884	Recently, we found that creatine kinase (CK) enzyme activity and CK-M subunit mRNA levels are decreased in the heart of rats with experimental diabetes mellitus.
64	1887884	The CK-M and CK-B genes are expressed in the heart, and we wanted to determine whether diabetes also induces a change in CK-B mRNA levels.
65	1887884	Quantitation of CK-M and CK-B mRNA levels on Northern blots with specific cDNA probes showed that, in diabetic hearts, CK-B mRNA levels represent only 19.8% of control levels and are more markedly depressed than CK-M mRNA levels, which are 46.5% of control values.
66	1887884	Acute injection of insulin led to a significant 1.6-fold increase in CK-M mRNA and a 2.2-fold increase of CK-B mRNA 5 h after insulin injection.
67	1887884	CK-M mRNA levels were restored to normal within 12 h, but 48 h were required to restore CK-B mRNA levels to normal values.
68	1887884	After 1 mo of insulin therapy, CK-B mRNA levels had risen 9.7-fold, exceeding normal values by 90%, whereas CK-M mRNA levels were at the normal level as previously shown.
69	1887884	Diabetes leads therefore to a marked lowering of CK-M and CK-B mRNA levels in the rat heart.
70	2679131	Several of the adenosinetriphosphatase enzymes that are responsible for cardiac muscle contraction rely on high-energy phosphates supplied by the creatine kinase (CK) system.
71	2679131	Chronic insulin therapy for 1 mo restores CK-M mRNA levels and enzyme activity.
72	3893798	The value for total serum creatine kinase (EC 2.7.3.2; CK) was 737 U/L (reference interval: 22-269 U/L), and electrophoresis for CK isoenzymes demonstrated two bands, the more anodal migrating to the CK-MB region and the second migrating between the CK-MB and CK-MM regions.
73	7808456	Unlike cytosolic muscle CK (MCK) and brain CK (BCK), there is no developmental isoenzyme switch between the MtCKs.
74	7808456	Cell culture models representing the tissue-specific expression of either sMtCK or uMtCK are available, but there are no adequate developmental models to examine their regulation.
75	7808456	Several animal models are available to examine the coordinate regulation of the CK gene family and include 1) Cardiac Stress by coarctation (sMtCK, BCK, and MCK), 2) Uterus and placenta during pregnancy (uMtCK and BCK), and 3) Diabetes and mitochondrial myopathy (sMtCK, BCK, and MCK).
76	7808456	Unlike cytosolic muscle CK (MCK) and brain CK (BCK), there is no developmental isoenzyme switch between the MtCKs.
77	7808456	Cell culture models representing the tissue-specific expression of either sMtCK or uMtCK are available, but there are no adequate developmental models to examine their regulation.
78	7808456	Several animal models are available to examine the coordinate regulation of the CK gene family and include 1) Cardiac Stress by coarctation (sMtCK, BCK, and MCK), 2) Uterus and placenta during pregnancy (uMtCK and BCK), and 3) Diabetes and mitochondrial myopathy (sMtCK, BCK, and MCK).
79	7954032	Abnormalities in systole and diastole related to lowering of CK-M and CK-B mRNA levels are normalized following insulin therapy.
80	9277555	Transgenic (Tg) FVB/N mice were produced that overexpress human lipoprotein lipase (LPL) in skeletal muscle using the muscle creatine kinase promoter and enhancers.
81	15047625	This study evaluates the role of oxidative stress in muscle-specific gene regulatory regions and myosin chain synthesis in streptozotocin (STZ)-induced diabetic and ZDF rats.
82	15047625	Myogenic regulatory factors--Myo, myogenin, and Jun D--were also reduced, and muscle enhancer factor (MEF)-1 DNA binding activity was impaired.
83	15047625	Moreover, synthesis of muscle creatine kinase and both heavy and light chains of myosin were impaired, suggesting that oxidative stress triggers the cascade of events that leads to impaired muscle repair.
84	15047625	When it was administered to diabetic rats, in addition to an improved oxidative imbalance there was a recovery of myogenic factors, MEF-1 DNA binding activity, synthesis of muscle creatine kinase, and myosin light and heavy chains.
85	15047625	This study evaluates the role of oxidative stress in muscle-specific gene regulatory regions and myosin chain synthesis in streptozotocin (STZ)-induced diabetic and ZDF rats.
86	15047625	Myogenic regulatory factors--Myo, myogenin, and Jun D--were also reduced, and muscle enhancer factor (MEF)-1 DNA binding activity was impaired.
87	15047625	Moreover, synthesis of muscle creatine kinase and both heavy and light chains of myosin were impaired, suggesting that oxidative stress triggers the cascade of events that leads to impaired muscle repair.
88	15047625	When it was administered to diabetic rats, in addition to an improved oxidative imbalance there was a recovery of myogenic factors, MEF-1 DNA binding activity, synthesis of muscle creatine kinase, and myosin light and heavy chains.
89	16513827	Recombinant human insulin-like growth factor-I treatment inhibits gluconeogenesis in a transgenic mouse model of type 2 diabetes mellitus.
90	16513827	IGF-I and insulin are structurally related polypeptides that mediate a similar pattern of biological effects via receptors that display considerably homology.
91	16513827	Administration of recombinant human IGF-I (rhIGF-I) has been proven to improve glucose control and liver and muscle insulin sensitivity in patients with type 2 diabetes mellitus (DM).
92	16513827	The effect of rhIGF-I treatment was evaluated in a mouse model of type 2 DM (MKR mouse), which expresses a dominant-negative form of the human IGF-I receptor under the control of the muscle creatine kinase promoter specifically in skeletal muscle.
93	16513827	MKR mice have impaired IGF-I and insulin signaling in skeletal muscle, leading to severe insulin resistance in muscle, liver, and fat, developing type 2 DM at 5 wk of age.
94	16513827	Also, these results suggest that a functional IGF-I receptor in skeletal muscle is required for IGF-I to improve insulin sensitivity in this mouse model of type 2 DM.
95	18979206	The forward reaction using ATP to generate phosphocreatine was reduced, while the reverse reaction using phosphocreatine to generate ATP was increased following dephosphorylation of immunoprecipitated M-CK with protein phosphatase 2A (PP2A) or PP2C.
96	21178104	In this study, bitransgenic mice were generated that overexpressed NCOAT(GK), an O-GlcNAcase-inactive spliced variant of the O-GlcNAcase gene, specifically in skeletal muscle using the muscle creatine kinase promoter.
97	22825472	We used the MCK(m)-hLPL mouse distinguished by skeletal and cardiac muscle-specific human lipoprotein lipase (hLPL) overexpression to investigate effects of lipid overload in skeletal muscle.