ライフサイエンスコーパス: GMF

1 GMF debranches filaments by a mechanism related to cofil

2 GMF does not bind monomeric ATP- or ADP-actin, confirmin

3 GMF induced two distinct open conformations of Arp2/3 co

4 GMF is implicated in both Arp2/3 debranching and inhibit

5 GMF promotes the differentiation of mammalian glia and n

6 GMF+/+ (Wt) mice developed severe EAE with a maximal mea

7 GMF-deficient mice showed reduced glial activation and s

8 GMF-null mice developed normally without gross abnormali

9 8, P < 0.001; T(1) r = -0.59, P = 0.002) and GMF (T(2) r = -0.73, P < 0.001; T(1) r = -0.53, P = 0.00

10 Therefore, ADF/cofilin and GMF, members of the same superfamily, appear to have evo

11 y effects on Arp2/3 complex with Coronin and GMF.

12 nstrate the critical role of GMF in EAE, and GMF antibody as a potent anti-inflammatory therapeutic a

13 system (CNS) of GMF+/+ (wild type) mice and GMF-/- (GMF-knockout) mice at the peak of EAE induced by

14 lization of GMF with four injections of anti-GMF antibody 5 to 11 days post immunization delayed the

15 3 networks are remodeled by proteins such as GMF, which blocks the actin-Arp2/3 interaction [4, 5], a

16 growth factor, glia maturation factor-beta (GMF).

17 e mice revealed profound differences between GMF-antibody treated mice and isotype matched control-an

18 examined the potential relationship between GMF or lack of it with learning and memory using the T-m

19 the daughter filament, suggesting that both GMF and cofilin can work by destabilizing the mother fil

20 ltiple sclerosis with control subjects, BPF, GMF and WMF were significantly reduced (P < 0.001 for al

21 n-promoting factor N-WASP is not affected by GMF, whereas nucleation activated by the WCA region of W

22 on the regulation of MAP kinase cascades by GMF.

23 es activation of the death domain caspase by GMF overexpression.

24 l ionic conditions to observe debranching by GMF and cofilin.

25 -defective adenovirus construct of GMF cDNA (GMF-V) induced overexpression of GMF protein in neurobla

26 In cultured S2R(+) cells, GMF silencing resulted in an increase in the width of la

27 We found that S. cerevisiae GMF (also called Aim7) localizes in vivo to cortical act

28 gh affinity (K(D) = 1.4 nM) to S. cerevisiae GMF (Gmf1), and together they form a stable ternary Crn1

29 obtained from the GMF-transfected cells (CM-GMF) and tested on primary neuronal cultures, consisting

30 ntribute to the neuroprotective effect of CM-GMF.

31 or, eliminated the neurotrophic effect of CM-GMF; whereas anti-NGF antibody was ineffective in preven

32 ted the RT-PCR results and indicated that CM-GMF contained greater concentrations of BDNF and NGF pro

33 We demonstrated that the CM-GMF had an enhanced neurotrophic effect as well as an in

34 tin disassembly-promoting proteins (cofilin, GMF, twinfilin, Srv2/CAP, coronin, AIP1, capping protein

35 In conclusion, GMF upregulates the expression of BDNF and NGF in C6 cel

36 sed Abeta1-42 in the brain of GMF-deficient (GMF-KO) mice, recently prepared in our laboratory.

37 branch stabilizer cortactin and destabilizer GMF each have a similar impact on SPIN90-activated Arp2/

38 nd a likely photoreceptor of the directional GMF response.

39 order of departure could be resolved during GMF- or cofilin-induced debranching, the Arp2/3 complex

40 dded generalized molecular fractionation (EE-GMF) method, a method based on the systematic fragmentat

41 ngle molecular or QM/MM calculations, the EE-GMF method shows significantly improved accuracy, nearly

42 emonstrate that neutralization of endogenous GMF with an affinity purified GMF antibody significantly

43 several protein kinases, and that endogenous GMF is rapidly phosphorylated upon stimulation of astroc

44 etween actin-WCA and glia maturation factor (GMF) for binding to Arp2/3 complex suggests that during

45 t over-expression of glia maturation factor (GMF) in glial cells cause excessive production and secre

46 Glia maturation factor (GMF) is a cofilin family protein that binds to the Arp2/

47 Glia maturation factor (GMF) is a member of the actin-depolymerizing factor (ADF

48 Glia maturation factor (GMF) is a unique brain protein localized in astrocytes a

49 at the brain protein glia maturation factor (GMF) is involved in intracellular signaling in glia.

50 ly demonstrated that glia maturation factor (GMF), a 17-kDa brain protein, can be phosphorylated in t

51 ort that recombinant glia maturation factor (GMF), a 17-kDa brain protein, inhibits the activity of m

52 rved previously that glia maturation factor (GMF), a 17-kDa brain protein, is rapidly phosphorylated

53 Glia maturation factor (GMF), a protein primarily localized in the central nervo

54 inhibitory ligands: glia maturation factor (GMF), Coronin, and Arpin.

55 Glia maturation factor (GMF), discovered and characterized in our laboratory, is

56 The protein glia maturation factor (GMF), which accelerates debranching, prevents branch ren

57 We show that glia-maturation factor (GMF), which is an Arp2/3 complex inhibitor and actin fil

58 the yeast homolog of glia maturation factor (GMF), which is structurally related to the actin filamen

59 family: cofilin and glial maturation factor (GMF).

60 olog of ADF/cofilin, glia maturation factor (GMF).

61 The geomagnetic field (GMF) is one of the environmental stimuli that plants exp

62 ient care between the General Medical Floor (GMF), Intensive Care Units (ICU) and Telemetry Unit (TU)

63 eraction with ADF/cofilin support a role for GMF in promoting the remodeling and/or disassembly of br

64 ted with the two suggested binding sites for GMF.

65 ter fraction (WMF) and grey matter fraction (GMF).

66 y (BPQ) was identified between patients from GMF and TU (OR 0.96; 95%CI 0.61, 1.52).

67 ental delay; 18/21 had gross motor function (GMF) impairment with GMF III or worse in 5/18, 16/16 int

68 Further, GMF inhibits nucleation of new daughter filaments.

69 Furthermore, GMF phosphorylated by protein kinase C (PKC), but not by

70 Furthermore, GMF synergized with Coronin in inhibiting actin nucleati

71 (CNS) of GMF+/+ (wild type) mice and GMF-/- (GMF-knockout) mice at the peak of EAE induced by immuniz

72 egion of WAVE2 is slightly inhibited at high GMF concentrations.

73 However, GMF lacks detectable actin binding or severing activity

74 8 carry out opposing functions and implicate GMF as a regulator of major cellular events.

75 The structural abnormality in GMF-null mice explained their impaired ability for both

76 Change in GMF correlated only modestly with the change in T2 lesio

77 This activity and mechanism are conserved in GMF homologs from evolutionarily distant species.

78 flammation and demyelination was detected in GMF-antibody-treated mice at days 8, 16, and 24 post imm

79 sed incidence and reduced severity of EAE in GMF-antibody-treated mice was consistent with the signif

80 s show that memory retention was improved in GMF-KO mice compared to Wt controls following Abeta infu

81 s undergoing guided migration was reduced in GMF mutant flies.

82 The phosphomimetic mutation S2E in GMF inhibits this interaction.

83 nd F-actin binding site on cofilin, which in GMF appears to contact the first actin subunit in the da

84 e growth factor from PC12 leads to increased GMF phosphorylation with a time course similar to that r

85 opy, 47.4% were admitted into TU, 43.7% into GMF and 8.9% into ICU.

86 Depletion of GMF gene by introducing GMF-specific siRNA (GsiRNA) completely blocked both acti

87 We demonstrate that cofilin, like GMF, is an authentic debrancher independent of its filam

88 Brugia malayi GMF (BmGMF) is also related to a large family of eukaryo

89 ty and mechanism are conserved for mammalian GMF.

90 thermal titration calorimetry that mammalian GMF has very low affinity for ATP-bound Arp2/3 complex b

91 d whether this activity extends to mammalian GMF have remained open questions.

92 This study investigated whether or not GMF plays a role in the survival-promoting and neuroprot

93 border cells is diminished in the absence of GMF.

94 hing, suggesting that the higher affinity of GMF for ADP-Arp2/3 complex plays a physiological role by

95 It appears that the mutual augmentation of GMF and PKA, and the stimulating effect of PKC, both ser

96 of AD, we infused Abeta1-42 in the brain of GMF-deficient (GMF-KO) mice, recently prepared in our la

97 lammatory cytokines/chemokines in the CNS of GMF-KO mice and increased expression in Wt mice with EAE

98 ators in the central nervous system (CNS) of GMF+/+ (wild type) mice and GMF-/- (GMF-knockout) mice a

99 3-dependent site of Tau was a consequence of GMF-overexpression in N18 cells.

100 eplication-defective adenovirus construct of GMF cDNA (GMF-V) induced overexpression of GMF protein i

101 ese Abeta1-42 effects in primary cultures of GMF-KO astrocyte and microglia were reversed by reconsti

102 Depletion of GMF gene by introducing GMF-specific siRNA (GsiRNA) comp

103 er deals with the behavior of mice devoid of GMF protein (knockout).

104 fically for making the device, mini-discs of GMF (d = 0.5 cm or any other shape and size) are machine

105 orward in deciphering the in vivo effects of GMF and supports the interaction of underlying mechanism

106 were reversed by reconstituted expression of GMF.

107 se (RSK) enhances the inhibitory function of GMF on ERK; protein kinase C (PKC) and casein kinase II

108 Immunoprecipitation of GMF from cell extracts using its specific antibody copre

109 wo factors play a role in the interaction of GMF with Arp2/3 complex.

110 he generation of various phospho-isoforms of GMF may explain its modulation of signal transduction at

111 ivation and large increases in the levels of GMF as well as induction of inflammatory cytokine/chemok

112 Neutralization of GMF with four injections of anti-GMF antibody 5 to 11 da

113 ee of fifteen Wt mice as compared to none of GMF-KO mice died of EAE.

114 Overexpression of GMF also increased caspase-3 activity, an early marker o

115 f GMF cDNA (GMF-V) induced overexpression of GMF protein in neuroblastoma (N18) cells caused cytotoxi

116 Studies with overexpression of GMF using adenovirus vector have uncovered its regulator

117 A preliminary phosphorylation of GMF by protein kinase A (PKA) dramatically increases its

118 d p38 is supported by the phosphorylation of GMF upon cellular stimulation by forskolin (blocked by P

119 The biphasic dose response of GMF-responsive genes indicates a hormetic response of pl

120 ese results demonstrate the critical role of GMF in EAE, and GMF antibody as a potent anti-inflammato

121 r results indicate a novel mediatory role of GMF in the neuro-inflammatory pathway of Abeta and its p

122 The set of GMF-regulated genes strongly overlapped with various str

123 containing putative phosphorylation sites of GMF, we demonstrate that PKA is capable of phosphorylati

124 Non-phosphorylated GMF or GMF phosphorylated by other kinases exhibits only minima

125 methane, while the remainder of the original GMF substrate is rendered superhydrophobic by reacting w

126 The transfected cells overexpressed GMF intracellularly, but did not secrete the protein.

127 reagents on photolithographically patterned GMF/paper).

128 e other three enzymes that can phosphorylate GMF, only p90 ribosomal S6 kinase (RSK) enhances the inh

129 Non-phosphorylated GMF or GMF phosphorylated by other kinases exhibits only

130 d that protein kinase A (PKA)-phosphorylated GMF is a potent inhibitor (IC50 = 3 nM) of the ERK1/ERK2

131 d that protein kinase A (PKA)-phosphorylated GMF is a potent inhibitor of extracellular signal-regula

132 we present evidence that PKA-phosphorylated GMF also promotes (11-fold) the catalytic activity of PK

133 The inhibitory effect of PKA-phosphorylated GMF is specific, as it does not suppress the activity of

134 report that, by contrast, PKA-phosphorylated GMF strongly enhances the activity of a related but dist

135 The inhibition of ERK by PKA-phosphorylated GMF suggests that GMF could be one of the mediators of t

136 On the other hand, that RSK-phosphorylated GMF also inhibits ERK implies a negative feedback loop i

137 The intracellular interaction of PKA, GMF, and p38 is supported by the phosphorylation of GMF

138 GSK-3beta, and lithium completely prevented GMF-dependent activation of caspase-3.

139 of endogenous GMF with an affinity purified GMF antibody significantly decreased the inflammation, s

140 cells from Wt mice transferred to recipient GMF-KO mice caused very mild and with low incidence of E

141 n-activated protein (MAP) kinase, suggesting GMF as a bifunctional regulator of the MAP kinase cascad

142 rthermore, genetic studies demonstrated that GMF cooperates with the Drosophila homolog of Aip1 (flar

143 Previously we demonstrated that GMF is required in the induced production of proinflamma

144 We previously demonstrated that GMF mediates the experimental autoimmune encephalomyelit

145 escent wave microscopy, we demonstrated that GMF potently stimulates debranching of actin filaments p

146 To test the hypothesis that GMF is involved in the pathogenesis of AD, we infused Ab

147 Taken together our results imply that GMF is involved in the signaling leading to the activati

148 We further show that GMF binds to the Arp2/3 complex with low nanomolar affin

149 ection fluorescence microscopy, we show that GMF depends on two separate surfaces for debranching.

150 en together, these observations suggest that GMF and cofilin promote debranching by distinct yet comp

151 Together, these data suggest that GMF binds Arp2/3 complex to both "prune" daughter filame

152 Together, the results suggest that GMF functions by a mechanism similar to that of other AD

153 These data suggest that GMF functions in vivo to promote the disassembly of Arp2

154 Our data suggest that GMF play a critical role in CNS inflammation.

155 ERK by PKA-phosphorylated GMF suggests that GMF could be one of the mediators of the suppressive eff

156 RT-PCR verified that GMF-transfected C6 cells had increased mRNA levels for B

157 This has been accomplished by activating the GMF surface through the self-assembly of propargyl-PEG3-

158 nes that are differentially regulated by the GMF in shoot and roots.

159 onditioned medium (CM) was obtained from the GMF-transfected cells (CM-GMF) and tested on primary neu

160 The decrease in glial activation in the GMF-KO mice is also associated with significant reductio

161 uously on Earth; however, the actions of the GMF on plants are poorly understood.

162 tional response to periodic rotations of the GMF vector in two insect species.

163 s, suggesting that both organs can sense the GMF.

164 We found that the GMF regulated genes in both shoot and roots, suggesting

165 however, plants can sense and respond to the GMF using the signaling networks involved in stress resp

166 dicates a hormetic response of plants to the GMF.

167 tionary advantage of plant adaptation to the GMF; however, plants can sense and respond to the GMF us

168 adequate bowel preparation when compared to GMF (Odds Ratio [OR] 0.36; 95% Confidence Interval [CI]

169 Modulation of GMFbeta, a ubiquitous GMF isoform, by depletion or overexpression resulted in

170 n decrease in grey matter fractional volume (GMF, as a fraction of total intracranial volume) was -0.

171 However, with beam walking, GMF-knockout mice performed poorly and failed to learn.

172 disassembly of aged actin filaments, whereas GMF interacts specifically with Arp2/3 complex at branch

173 6+/-0.5 by day 16 post-immunization, whereas GMF-KO mice showed significantly delayed EAE with an ave

174 protective effects, we investigated whether GMF-transfection upregulated the expression of neurotrop

175 d to cofilin-mediated severing, but in which GMF has evolved to target molecular junctions between ac

176 While GMF binds directly to the Arp2/3 complex, cofilin select

177 d gross motor function (GMF) impairment with GMF III or worse in 5/18, 16/16 intellectual disability,

178 n of GSK-3beta occurred after infection with GMF-V when compared with mock and lacZ controls.

179 nd by the co-immunoprecipitation of p38 with GMF from cell lysates.

180 glioma cells were transfected in vitro with GMF utilizing an adenovirus vector.

181 re sensitive to debranching by fission yeast GMF (glia maturation factor) than branches with ADP-P (i