Ignet

Gene Information

Gene symbol: MBP

Gene name: myelin basic protein

HGNC ID: 6925

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	AKT1	1 hits
3	ATP1A2	1 hits
4	CCHCR1	1 hits
5	CD4	1 hits
6	COL1A1	1 hits
7	DBP	1 hits
8	F2	1 hits
9	GFAP	1 hits
10	GRP	1 hits
11	HLA-A	1 hits
12	HSD11B1	1 hits
13	IDDM2	1 hits
14	IFNG	1 hits
15	IL10	1 hits
16	IL2	1 hits
17	INS	1 hits
18	INSR	1 hits
19	MAPK1	1 hits
20	ME1	1 hits
21	MYH14	1 hits
22	NEFH	1 hits
23	NGF	1 hits
24	NGFR	1 hits
25	NOS2A	1 hits
26	PDE5A	1 hits
27	PLP1	1 hits
28	PPP1R12A	1 hits
29	PROX1	1 hits
30	RAG2	1 hits
31	RHOA	1 hits
32	RHOD	1 hits
33	S100A1	1 hits
34	SNAP25	1 hits
35	TG	1 hits
36	TGFB1	1 hits
37	THRA	1 hits
38	THRSP	1 hits
39	TPO	1 hits

Related Sentences

#	PMID	Sentence
1	1321840	Hepatic PTPase activity was measured using two artificial substrates phosphorylated on tyrosine: reduced, carboxyamidomethylated, and maleylated lysozyme (P-Tyr-RCML) and myelin basic protein (P-Tyr-MBP), as well as an autophosphorylated 48-kD insulin receptor tyrosine kinase domain (P-Tyr-IRKD).
2	1717849	The mechanism of cell damage associated with aberrant MHC molecule expression is unclear: for example, overexpression of class I and class II MHC molecules in pancreatic beta cells in transgenic mice leads to nonimmune destruction of the cells and insulin-dependent diabetes mellitus.
3	1717849	We have generated transgenic mice that express class I H-2Kb MHC molecules, under the control of the myelin basic protein promoter, specifically in oligodendrocytes.
4	1720778	Co-transfection of MBP (-256/+1)-chloramphenicol acetyltransferase chimeric gene with a plasmid expressing thyroid hormone receptor alpha, and in the presence of 3,5,3'-triiodothyronine, into NIH3T3 or NG108-15, increased chloramphenicol acetyltransferase expression 4-fold.
5	1720778	Our finding of a specific hormone-receptor interaction with the MBP promoter region is the first direct demonstration of a thyroid hormone-responsive element in a brain-specific gene.
6	1720778	Co-transfection of MBP (-256/+1)-chloramphenicol acetyltransferase chimeric gene with a plasmid expressing thyroid hormone receptor alpha, and in the presence of 3,5,3'-triiodothyronine, into NIH3T3 or NG108-15, increased chloramphenicol acetyltransferase expression 4-fold.
7	1720778	Our finding of a specific hormone-receptor interaction with the MBP promoter region is the first direct demonstration of a thyroid hormone-responsive element in a brain-specific gene.
8	1946445	Oral administration of the autoantigens myelin basic protein and collagen type II suppresses experimental models of encephalomyelitis and arthritis.
9	7505909	Insulin treatment normalizes glycemia levels, partially counteracts P0 mRNA increase at both stages of diabetes and delays MBP mRNA increase present only in chronic animals.
10	7505909	We suggest that increased transcript levels of P0 and MBP in Schwann cells may represent a higher turnover of myelin sheath specific proteins in diabetic syndrome, as attempt to repair the hyperglycemia-induced nerve damage, which is partially prevented by insulin treatment.
11	7505909	Insulin treatment normalizes glycemia levels, partially counteracts P0 mRNA increase at both stages of diabetes and delays MBP mRNA increase present only in chronic animals.
12	7505909	We suggest that increased transcript levels of P0 and MBP in Schwann cells may represent a higher turnover of myelin sheath specific proteins in diabetic syndrome, as attempt to repair the hyperglycemia-induced nerve damage, which is partially prevented by insulin treatment.
13	7515882	Stimulation of protein phosphatase-1 activity by phorbol esters.
14	7515882	Evaluation of the regulatory role of protein kinase C in insulin action.
15	7515882	In this study, we examined the role of insulin, protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) cascade in activation of protein phosphatase-1 (PP-1) by using three complementary approaches.
16	7515882	The PP-1 stimulation by TPA was comparable to stimulation by insulin (t1/2 = 1 min and EC50 = 5 nM) with a maximum effect in 5 min.
17	7515882	Insulin and TPA also stimulated MAPK (> 2-fold increase over basal, with myelin basic protein as a substrate).
18	7515882	ML-9, a myosin light chain kinase inhibitor, blocked the effects of insulin and TPA on both MAPK and PP-1 activation.
19	7515882	In these cells subsequent effects of insulin on MAPK and PP-1 activation were blocked, without an effect on basal enzyme levels.
20	7515882	These inhibitors completely prevented insulin and TPA stimulation of MAPK and PP-1 and blocked insulin-induced translocation of PKC to the plasma membranes.
21	7515882	We conclude that PKC plays an important role in insulin stimulation of PP-1 via the activation of MAPK cascade.
22	8644999	Addition of zinc chloride to bombesin-sensitive Swiss 3T3 mouse fibroblasts induced a fourfold stimulation in the cytosolic myelin basic protein kinase activity.
23	8644999	The kinase activity coeluted with p42 MAP kinase using chromatography on Mono-Q ion exchange.
24	8644999	Immunoprecipitation against the p85 subunit of phosphatidylinositol 3-kinase resulted in the appearance of two phosphotyrosine-containing proteins, 100 and 115 kDa, in extracts from cells treated with zinc or epidermal growth factor, indicating that the tyrosine phosphorylation was recognized by the corresponding SH2-domains.
25	8644999	The present study demonstrates that extracellular zinc has the potential to partially mimic the action of growth factors on intracellular MAP kinase activation and protein tyrosine phosphorylation.
26	8705860	Analysis of T cells reacting to the pathogenic portion of the MBP molecule indicated that in the vaccinated mice there was a reduction in the Th1 cytokines interleukin-2 (IL-2) and interferon-gama.
27	8811061	Administration of recombinant interleukin (IL)-2 was shown to reverse the tolerance induced by feeding low doses of MBP, but not the tolerance induced by feeding high doses of MBP, indicating that deletion had occurred in the high-dose group.
28	8892082	In contrast to expectations, the peptide was found to augment not only EAE induced by MBP-specific T cells, but also proteolipid protein (PLP)-specific T cell- or PLP peptide-induced EAE in SJL/J mice, and MBP-induced EAE and adjuvant arthritis (AA) in rats.
29	9231779	The present work reports the identification of a novel nuclear protein from 19-day-old embryonic rat brain that displays a distinct interaction pattern with TR isoforms at the level of the TRE of two genes known to be differentially expressed and regulated by thyroid hormone (T3): the ubiquitous malic enzyme and the brain-specific myelin basic protein.
30	9231779	Electrophoretic gel mobility shift assays demonstrate that only TRbeta1 forms a specific complex with the rat brain nuclear factor on the myelin basic protein-TRE, but not on the malic enzyme-TRE.
31	9231779	The present work reports the identification of a novel nuclear protein from 19-day-old embryonic rat brain that displays a distinct interaction pattern with TR isoforms at the level of the TRE of two genes known to be differentially expressed and regulated by thyroid hormone (T3): the ubiquitous malic enzyme and the brain-specific myelin basic protein.
32	9231779	Electrophoretic gel mobility shift assays demonstrate that only TRbeta1 forms a specific complex with the rat brain nuclear factor on the myelin basic protein-TRE, but not on the malic enzyme-TRE.
33	9348197	Structural requirements for the inhibitory action of thyroid hormone receptor splicing variant alpha2 (TR alpha2) on T3/TRbeta1-mediated transactivation were investigated in native promoters of two T3-regulated genes: the brain-specific myelin basic protein (MBP) and the housekeeping malic enzyme (ME).
34	9637504	In the murine autoimmune diseases experimental autoimmune encephalomyelitis and collagen-induced arthritis, MHC class II molecules I-Au and I-Aq present peptides derived from myelin basic protein and type II collagen, respectively, to autoreactive T cells.
35	9652824	Peptides derived from thyroid peroxidase, HLA-DQ(alpha10301), HLA-DQ(alpha10302), retinol receptor and p21ras were among the high-affinity binders, whereas peptides derived from myelin basic protein were among the low-affinity binders.
36	9776708	Insulin, thyroglobulin and myelin basic protein (MBP) are implicated as autoantigens in the autoimmune diseases, insulin-dependent diabetes mellitus (IDDM), autoimmune thyroid-disease and multiple sclerosis.
37	9776708	Expression was examined in mRNA isolated from complete adult rat thymus, various mouse thymic cell-types isolated from fetal thymic-organ cultures and from neonatal-mouse thymocyte subsets. mRNA for insulin, thyroglobulin and MBP were detected in unfractionated adult rat and embryonic mouse thymus.
38	9776708	Thyroglobulin and MBP, but not insulin mRNA were detected in mouse MHC class II+ thymic epthelial cells and class II+ dendritic cells and in certain thymocyte subsets.
39	9776708	The presence of insulin, thyroglobubin and MBP mRNA in the thymus has important implications for the development of the T-cell repertoire, particularly for the mechanisms of tolerance that prevent autoreactivity to these antigens in healthy individuals.
40	9776708	Insulin, thyroglobulin and myelin basic protein (MBP) are implicated as autoantigens in the autoimmune diseases, insulin-dependent diabetes mellitus (IDDM), autoimmune thyroid-disease and multiple sclerosis.
41	9776708	Expression was examined in mRNA isolated from complete adult rat thymus, various mouse thymic cell-types isolated from fetal thymic-organ cultures and from neonatal-mouse thymocyte subsets. mRNA for insulin, thyroglobulin and MBP were detected in unfractionated adult rat and embryonic mouse thymus.
42	9776708	Thyroglobulin and MBP, but not insulin mRNA were detected in mouse MHC class II+ thymic epthelial cells and class II+ dendritic cells and in certain thymocyte subsets.
43	9776708	The presence of insulin, thyroglobubin and MBP mRNA in the thymus has important implications for the development of the T-cell repertoire, particularly for the mechanisms of tolerance that prevent autoreactivity to these antigens in healthy individuals.
44	9776708	Insulin, thyroglobulin and myelin basic protein (MBP) are implicated as autoantigens in the autoimmune diseases, insulin-dependent diabetes mellitus (IDDM), autoimmune thyroid-disease and multiple sclerosis.
45	9776708	Expression was examined in mRNA isolated from complete adult rat thymus, various mouse thymic cell-types isolated from fetal thymic-organ cultures and from neonatal-mouse thymocyte subsets. mRNA for insulin, thyroglobulin and MBP were detected in unfractionated adult rat and embryonic mouse thymus.
46	9776708	Thyroglobulin and MBP, but not insulin mRNA were detected in mouse MHC class II+ thymic epthelial cells and class II+ dendritic cells and in certain thymocyte subsets.
47	9776708	The presence of insulin, thyroglobubin and MBP mRNA in the thymus has important implications for the development of the T-cell repertoire, particularly for the mechanisms of tolerance that prevent autoreactivity to these antigens in healthy individuals.
48	9776708	Insulin, thyroglobulin and myelin basic protein (MBP) are implicated as autoantigens in the autoimmune diseases, insulin-dependent diabetes mellitus (IDDM), autoimmune thyroid-disease and multiple sclerosis.
49	9776708	Expression was examined in mRNA isolated from complete adult rat thymus, various mouse thymic cell-types isolated from fetal thymic-organ cultures and from neonatal-mouse thymocyte subsets. mRNA for insulin, thyroglobulin and MBP were detected in unfractionated adult rat and embryonic mouse thymus.
50	9776708	Thyroglobulin and MBP, but not insulin mRNA were detected in mouse MHC class II+ thymic epthelial cells and class II+ dendritic cells and in certain thymocyte subsets.
51	9776708	The presence of insulin, thyroglobubin and MBP mRNA in the thymus has important implications for the development of the T-cell repertoire, particularly for the mechanisms of tolerance that prevent autoreactivity to these antigens in healthy individuals.
52	10203357	Protein kinase C (PKC), an enzyme known to be stimulated in DM, also activates MAPK.
53	10203357	MAPK activity, measured as myelin basic protein kinase, was elevated by approximately 50% in DM versus controls (CON).
54	10203357	Increased protein contents of p42mapk and p44mapk, as well as increased tyrosine phosphorylation and mobility shift of p42mapk, were also observed in DM.
55	10203357	Protein expression of MAPK phosphatase-1 (MKP-1), a dual specificity phosphatase that inactivates MAPK, was approximately 60% of CON.
56	10203357	These results demonstrate that glomerular MAPK is activated in DM by multiple mechanisms i.e., increases in protein contents, increased phosphorylation, and decreased dephosphorylation of the enzyme due to suppression of MKP-1.
57	10610182	In transgenic mice, we have expressed three human components involved in T-cell recognition of an MS-relevant autoantigen presented by the HLA-DR2 molecule: DRA0101/DRB11501 (HLA-DR2), an MHC class II candidate MS susceptibility genes found in individuals of European descent; a T-cell receptor (TCR) from an MS-patient-derived T-cell clone specific for the HLA-DR2 bound immunodominant myelin basic protein (MBP) 4102 peptide; and the human CD4 coreceptor.
58	10610182	When DR2 and TCR double-transgenic mice were backcrossed twice to Rag2 (for recombination-activating gene 2)-deficient mice, the incidence of spontaneous disease increased, demonstrating that T cells specific for the HLA-DR2 bound MBP peptide are sufficient and necessary for development of disease.
59	10610182	In transgenic mice, we have expressed three human components involved in T-cell recognition of an MS-relevant autoantigen presented by the HLA-DR2 molecule: DRA0101/DRB11501 (HLA-DR2), an MHC class II candidate MS susceptibility genes found in individuals of European descent; a T-cell receptor (TCR) from an MS-patient-derived T-cell clone specific for the HLA-DR2 bound immunodominant myelin basic protein (MBP) 4102 peptide; and the human CD4 coreceptor.
60	10610182	When DR2 and TCR double-transgenic mice were backcrossed twice to Rag2 (for recombination-activating gene 2)-deficient mice, the incidence of spontaneous disease increased, demonstrating that T cells specific for the HLA-DR2 bound MBP peptide are sufficient and necessary for development of disease.
61	10976915	Regulation of myosin-bound protein phosphatase by insulin in vascular smooth muscle cells: evaluation of the role of Rho kinase and phosphatidylinositol-3-kinase-dependent signaling pathways.
62	10976915	Insulin-mediated MBP activation was accompanied by a rapid time-dependent reduction in the phosphorylation state of the myosin-bound regulatory subunit (MBS) of MBP.
63	10976915	The decrease observed in MBS phosphorylation was due to insulin-induced inhibition of Rho kinase activity.
64	10976915	Insulin also prevented a thrombin-mediated increase in Rho kinase activation and abolished the thrombin-induced increase in MBS phosphorylation and MBP inactivation.
65	10976915	These data are consistent with the notion that insulin inactivates Rho kinase and decreases MBS phosphorylation to activate MBP in VSMCs.
66	10976915	Furthermore, treatment with synthetic inhibitors of phosphatidylinositol-3 kinase (PI3-kinase), nitric oxide synthase (NOS), and cyclic guanosine monophosphate (cGMP) all blocked insulin's effect on MBP activation.
67	10976915	We conclude that insulin stimulates MBP via its regulatory subunit, MBS partly by inactivating Rho kinase and stimulating NO/cGMP signaling via PI3-kinase as part of a complex signaling network that controls 20-kDa myosin light chain (MLC20) phosphorylation and VSMC contraction.
68	11369711	Treatment of (PL/J x SJL)F(1) mice with low-dose oral myelin basic protein (MBP) (0.5 mg) and simultaneous oral IL-10 given 3 times reduced the severity and incidence of experimental autoimmune encephalomyelitis (EAE), whereas administration of oral IL-10 alone or MBP alone given in these doses had no effect.
69	11369711	Lymphocytes from mice treated orally with MBP and IL-10 proliferated less, and produced decreased amounts of IFN-gamma and IL-2 and increased amounts of IL-10 and transforming growth factor-beta upon in vitro stimulation with MBP.
70	11369711	Nasal administration of antigen and IL-10 reduced proliferative responses and IFN-gamma production, increased IL-10 production, and enhanced protection from EAE.
71	11369711	In addition, oral IL-10 combined with oral myelin oligodendrocyte glycoprotein (MOG) 35-55 reduced relapses in MOG-induced EAE in the NOD mouse, as well as enhanced the protective effect of oral insulin in the NOD model of diabetes.
72	11369711	Treatment of (PL/J x SJL)F(1) mice with low-dose oral myelin basic protein (MBP) (0.5 mg) and simultaneous oral IL-10 given 3 times reduced the severity and incidence of experimental autoimmune encephalomyelitis (EAE), whereas administration of oral IL-10 alone or MBP alone given in these doses had no effect.
73	11369711	Lymphocytes from mice treated orally with MBP and IL-10 proliferated less, and produced decreased amounts of IFN-gamma and IL-2 and increased amounts of IL-10 and transforming growth factor-beta upon in vitro stimulation with MBP.
74	11369711	Nasal administration of antigen and IL-10 reduced proliferative responses and IFN-gamma production, increased IL-10 production, and enhanced protection from EAE.
75	11369711	In addition, oral IL-10 combined with oral myelin oligodendrocyte glycoprotein (MOG) 35-55 reduced relapses in MOG-induced EAE in the NOD mouse, as well as enhanced the protective effect of oral insulin in the NOD model of diabetes.
76	11509551	Selected contribution: insulin utilizes NO/cGMP pathway to activate myosin phosphatase via Rho inhibition in vascular smooth muscle.
77	11509551	Our laboratory has recently demonstrated that insulin induces relaxation of vascular smooth muscle cells (VSMCs) by activating myosin-bound phosphatase (MBP) and by inhibiting Rho kinase (Begum N, Duddy N, Sandu OA, Reinzie J, and Ragolia L.
78	11509551	In this study, we tested the hypothesis that insulin via the nitric oxide (NO)/cGMP pathway may inactivate Rho, resulting in a decrease in phosphorylation of the myosin-bound subunit (MBS(Thr695)) of MBP and in its activation.
79	11509551	Treatment of confluent serum-starved VSMCs with insulin prevented thrombin-induced increases in membrane-associated RhoA, Rho kinase activation, and site-specific phosphorylation of MBS(Thr695) of MBP and caused MBP activation.
80	11509551	Preexposure to N(G)-monomethyl-L-arginine, a NO synthase inhibitor, and R-p-8-(4-chlorophenylthio)cGMP, a cGMP antagonist, attenuated insulin's inhibitory effect on Rho translocation and restored thrombin-mediated Rho kinase activation and site-specific MBS(Thr695) phosphorylation, resulting in MBP inactivation.
81	11509551	In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked insulin's inhibitory effects by abolishing thrombin-mediated Rho signaling and promoted dephosphorylation of MBS(Thr695).
82	11509551	Furthermore, expression of a dominant-negative RhoA decreased basal as well as thrombin-induced MBS(Thr695) phosphorylation and caused insulin activation of MBP.
83	11509551	Collectively, these results indicate that insulin inhibits Rho signaling by decreasing RhoA translocation via the NO/cGMP signaling pathway to cause MBP activation via site-specific dephosphorylation of its regulatory subunit MBS.
84	11509551	Selected contribution: insulin utilizes NO/cGMP pathway to activate myosin phosphatase via Rho inhibition in vascular smooth muscle.
85	11509551	Our laboratory has recently demonstrated that insulin induces relaxation of vascular smooth muscle cells (VSMCs) by activating myosin-bound phosphatase (MBP) and by inhibiting Rho kinase (Begum N, Duddy N, Sandu OA, Reinzie J, and Ragolia L.
86	11509551	In this study, we tested the hypothesis that insulin via the nitric oxide (NO)/cGMP pathway may inactivate Rho, resulting in a decrease in phosphorylation of the myosin-bound subunit (MBS(Thr695)) of MBP and in its activation.
87	11509551	Treatment of confluent serum-starved VSMCs with insulin prevented thrombin-induced increases in membrane-associated RhoA, Rho kinase activation, and site-specific phosphorylation of MBS(Thr695) of MBP and caused MBP activation.
88	11509551	Preexposure to N(G)-monomethyl-L-arginine, a NO synthase inhibitor, and R-p-8-(4-chlorophenylthio)cGMP, a cGMP antagonist, attenuated insulin's inhibitory effect on Rho translocation and restored thrombin-mediated Rho kinase activation and site-specific MBS(Thr695) phosphorylation, resulting in MBP inactivation.
89	11509551	In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked insulin's inhibitory effects by abolishing thrombin-mediated Rho signaling and promoted dephosphorylation of MBS(Thr695).
90	11509551	Furthermore, expression of a dominant-negative RhoA decreased basal as well as thrombin-induced MBS(Thr695) phosphorylation and caused insulin activation of MBP.
91	11509551	Collectively, these results indicate that insulin inhibits Rho signaling by decreasing RhoA translocation via the NO/cGMP signaling pathway to cause MBP activation via site-specific dephosphorylation of its regulatory subunit MBS.
92	11739394	Active Rho kinase (ROK-alpha ) associates with insulin receptor substrate-1 and inhibits insulin signaling in vascular smooth muscle cells.
93	11739394	Recent studies from our laboratory have shown that insulin stimulates myosin-bound phosphatase (MBP) in vascular smooth muscle cells (VSMCs) by decreasing site-specific phosphorylation of the myosin-bound subunit (MBS) of MBP via nitric oxide/cGMP-mediated Rho/Rho kinase inactivation.
94	11739394	Here we tested potential interactions between Rho kinase and insulin signaling pathways.
95	11739394	In control VSMCs, insulin inactivates ROK-alpha, the major Rho kinase isoform in VSMCs, and inhibits thrombin-induced increase in ROK-alpha association with the insulin receptor substrate-1 (IRS-1).
96	11739394	Hypertension (in spontaneous hypertensive rats) or expression of an active RhoA(V14) up-regulates Rho kinase activity and increases ROK-alpha/IRS-1 association resulting in IRS-1 serine phosphorylation that leads to inhibition of both insulin-induced IRS-1 tyrosine phosphorylation and phosphatidylinositol 3-kinase (PI3-kinase) activation.
97	11739394	In contrast, expression of dominant negative RhoA or cGMP-dependent protein kinase type I alpha inactivates Rho kinase, abolishes ROK-alpha/IRS-1 association, and potentiates insulin-induced tyrosine phosphorylation and PI3-kinase activation leading to decreased MBS(T695) phosphorylation and decreased MBP inhibition.
98	11739394	Collectively, these results suggest a novel function for ROK-alpha in insulin signal transduction at the level of IRS-1 and potential cross-talk between cGMP-dependent protein kinase type I alpha, Rho/Rho kinase signaling, and insulin signaling at the level of IRS-1/PI3-kinase.
99	12957877	Myosin bound phosphatase (MBP) dephosphorylates myosin light chains which play a dominant role in vascular smooth muscle (VSM) contraction.
100	12957877	Using two distinct approaches, we have demonstrated that insulin rapidly stimulates MBP and simultaneously inhibits RhoA/Rho kinase signaling via the nitric oxide (NO)/cGMP signaling pathway.
101	12957877	Insulin activates MBP by decreasing Thr695 phosphorylation of myosin-bound subunit (MBS) via two different but cross-talking signaling pathways.
102	12957877	Secondly, insulin induces iNOS expression via PI3-kinase signaling leading to generation of NO/cGMP which activates MBP via cGK-1( mediated inhibition of MBSThr695 phosphorylation via Rho kinase inactivation.
103	12957877	The defects appear to be at the level of PI3-kinase activation due to impaired insulin-induced IRS-1 tyrosine phosphorylation because of increased association of active Rho kinase with the IRS-1 leading to increased IRS-1 serine phosphorylation, which interrupts with downstream insulin signaling.
104	12957877	Myosin bound phosphatase (MBP) dephosphorylates myosin light chains which play a dominant role in vascular smooth muscle (VSM) contraction.
105	12957877	Using two distinct approaches, we have demonstrated that insulin rapidly stimulates MBP and simultaneously inhibits RhoA/Rho kinase signaling via the nitric oxide (NO)/cGMP signaling pathway.
106	12957877	Insulin activates MBP by decreasing Thr695 phosphorylation of myosin-bound subunit (MBS) via two different but cross-talking signaling pathways.
107	12957877	Secondly, insulin induces iNOS expression via PI3-kinase signaling leading to generation of NO/cGMP which activates MBP via cGK-1( mediated inhibition of MBSThr695 phosphorylation via Rho kinase inactivation.
108	12957877	The defects appear to be at the level of PI3-kinase activation due to impaired insulin-induced IRS-1 tyrosine phosphorylation because of increased association of active Rho kinase with the IRS-1 leading to increased IRS-1 serine phosphorylation, which interrupts with downstream insulin signaling.
109	14609218	In several autoimmune models, feedback regulation employing both CD4+ and CD8+ T cells of TCR specificity can be shown to occur and to account for remission from the transient disease state, or for its prevention.
110	14609218	In this model, the acetylated 1-9 N-terminal antigenic determinant from myelin basic protein (MBP) induces a transient paralytic disease owing to the activation of self-directed, high-affinity, CD4+ T cells.
111	14609218	A CD4+ T cell directed against a TCR determinant in the framework region of the Vbeta chain, and a CD8+ T cell directed against an upstream, distinct framework determinant, both of which are necessary for regulation, bring about a reversal of the disease process.
112	15350486	Survival analysis to identify predictors of death was performed using the actuarial method, Cox proportional model, including systolic, diastolic, mean, and pulse blood pressures (SBP, DBP, MBP, PP).
113	15350486	None of the initial BP parameters (SBP, DBP, PP, MBP, hypertension stages) seemed to influence early or global mortalities, which were rather related to the urgent onset of renal replacement therapy, to age, to serum albumin, and to the score of associated morbidities.
114	16855220	AKT phosphorylation is essential for insulin-induced relaxation of rat vascular smooth muscle cells.
115	16855220	The role of Akt on insulin-induced relaxation of vascular smooth muscle cell (VSMC) was investigated using siRNA targeting Akt (siAKTc) and adenovirus constructing myristilated Akt to either suppress endogenous Akt or overexpress constitutively active Akt, respectively. siAKTc decreased both basal and insulin-induced phosphorylations of Akt and glycogen synthase kinase 3beta, abolishing insulin-induced nitric oxide synthase (iNOS) expression. cGMP-dependent kinase 1alpha (cGK1alpha) and myosin-bound phosphatase (MBP) activities, both downstream of iNOS, were also decreased. siAKTc treatment resulted in increased insulin and ANG II-stimulated phosphorylation of contractile apparatus, such as MBP substrate (MYPT1) and myosin light chain (MLC20), accompanied by increased Rho-associated kinase alpha (ROKalpha) activity, demonstrating the requirement of Akt for insulin-induced vasorelaxation.
116	16855220	Corroborating these results, constitutively active Akt upregulated the signaling molecules involved in insulin-induced relaxation such as iNOS, cGK1alpha, and MBP activity, even in the absence of insulin stimulation.
117	16855220	On the contrary, the contractile response involving the phosphorylation of MYPT1 and MLC20, and increased ROKalpha activity stimulated by ANG II were all abolished by overexpressing active Akt.
118	16855220	In conclusion, we demonstrated here that insulin-induced VSMC relaxation is dependent on Akt activation via iNOS, cGK1alpha, and MBP activation, as well as the decreased phosphorylations of MYPT1 and MLC20 and decreased ROKalpha activity.
119	17223273	Weekly behavioral testing began prior to streptozotocin (STZ) administration and continued until 8 weeks, at which time myelinated fiber innervation was examined in the footpad by immunohistochemistry using antiserum to neurofilament heavy chain (NF-H) and myelin basic protein (MBP).
120	17223273	To test whether two neurotrophins nerve growth factor (NGF) and/or neurotrophin-3 (NT-3) known to support myelinated cutaneous fibers could influence myelinated innervation, diabetic mice were treated intrathecally for 2 weeks with NGF, NT-3, NGF and NT-3.
121	17223273	Neurotrophin-treated mice were then compared with diabetic mice treated with insulin for 2 weeks.
122	17223273	NGF and insulin treatment both increased paw withdrawal to mechanical stimulation in diabetic mice, whereas NT-3 or a combination of NGF and NT-3 failed to alter paw withdrawal responses.
123	19227273	Immunohistochemical (tests for insulin, glucagons, periferin, SNAP-25, GFAP, NGF-R, RMR-22, MBP) and morphological studies were performed to examine the pancreatic nervous apparatus of human adults and fetuses in late phases of development.
124	19227273	The insular endocrine cells are shown to synthesize the proteins (SNAP-25, GFAP) characteristic of nerve cells and their synaptic terminals.
125	19470805	Haplotype mapping reduced the critical region of the distal part of the QTL to 31 Mbp containing the potential candidates Nr1i3, Apoa2, Atp1a2, Prox1, and Hsd11b1.
126	21820491	In diabetic mice, PDE5 expression in sciatic nerve tissue was significantly upregulated, whereas the myelin sheath thickness, myelin basic protein (MBP), and subcutaneous nerve fibers were significantly reduced.
127	21820491	In vitro, hyperglycemia upregulated PDE5 in Schwann cells and reduced Schwann cell proliferation, migration, and expression of brain-derived neurotrophic factor (BDNF).
128	23667870	Autoantibodies to neuron-specific proteins S100, GFAP, MBP and NGF in the serum of rats with streptozotocin-induced diabetes.
129	23667870	The appearance of autoantibodies to neuronal proteins (S100, GFAP, MBP, and NGF) in rat serum was analyzed by ELISA on days 5, 10, 17, 25, and 32 after streptozotocin injection.
130	23667870	The levels of antibodies to specific neuronal proteins (S100, GFAP, MBP, and NGF) also increased at this term.
131	23667870	Autoantibodies to neuron-specific proteins S100, GFAP, MBP and NGF in the serum of rats with streptozotocin-induced diabetes.
132	23667870	The appearance of autoantibodies to neuronal proteins (S100, GFAP, MBP, and NGF) in rat serum was analyzed by ELISA on days 5, 10, 17, 25, and 32 after streptozotocin injection.
133	23667870	The levels of antibodies to specific neuronal proteins (S100, GFAP, MBP, and NGF) also increased at this term.
134	23667870	Autoantibodies to neuron-specific proteins S100, GFAP, MBP and NGF in the serum of rats with streptozotocin-induced diabetes.
135	23667870	The appearance of autoantibodies to neuronal proteins (S100, GFAP, MBP, and NGF) in rat serum was analyzed by ELISA on days 5, 10, 17, 25, and 32 after streptozotocin injection.
136	23667870	The levels of antibodies to specific neuronal proteins (S100, GFAP, MBP, and NGF) also increased at this term.