ライフサイエンスコーパス: DGC

1 DGC activity of GcbA was required for its function, as a

2 DGC deficiency in humans results in muscular dystrophy,

3 DGCs have long been implicated in TLE, because they regu

4 DGCs were also labeled after injections into the anterio

5 nsport, more retrogradely labeled (P < 0.05) DGC propriospinal neurons (T13-S1) were quantified in in

6 with 3 or more cases of DGC; families with 1 DGC before the age of 40; and families with a history of

7 is represents the first description of (1) a DGC post-transcriptionally activated by direct pairing w

8 tation of the alpha-sarcoglycan gene, also a DGC component, causes LGMD2D and represents the most com

9 We determined that CdgH acts as a DGC and positively regulates rugosity, whereas CdgG does

10 xpressing newborn cells began to establish a DGC-like morphology at approximately 7 d after birth, wi

11 mple spindle-like morphology develops into a DGC, consisting of a single apical dendrite with further

12 ow that the inner membrane protein NicD is a DGC that controls dispersal by sensing nutrient levels:

13 inantly a PDE, while CdgB is predominantly a DGC.

14 ifferentially regulated DGCs revealed that a DGC, CdgA, is responsible for the increase in biofilm fo

15 o Alg44 (a PilZ protein) or regulate WspR (a DGC enzyme that has been shown to bind to dimeric c-di-G

16 ulnerability to SE, indicating that abnormal DGC plasticity derives exclusively from aberrantly devel

17 If abnormal DGCs do contribute, a reasonable prediction would be tha

18 or decades, direct evidence linking abnormal DGCs to seizures has been lacking.

19 While the presence of abnormal DGCs in epilepsy has been known for decades, direct evid

20 Here, we isolate the effects of abnormal DGCs using a transgenic mouse model to selectively delet

21 rrelated with the number or load of abnormal DGCs.

22 tion of the mTOR pathway, producing abnormal DGCs morphologically similar to those in epilepsy.

23 e in support of the hypothesis that abnormal DGCs contribute to the development of TLE and also suppo

24 s in about 4 weeks, confirming that abnormal DGCs, which are present in both animals and humans with

25 ulation-rather than the previously activated DGC ensembles that responded to past events-was selected

26 oreover, ECA3270 represents the first active DGC reported to have an alternative active-site motif fr

27 l neurons by increasing the firing of active DGCs.SIGNIFICANCE STATEMENT Adult brains are constantly

28 For the first time, we found that active DGCs responded to a novel experience by increasing their

29 ike OdaA, which did not significantly affect DGC activity of SadC, OdaI inhibited c-di-GMP production

30 doscopy and clinicopathology between PGC and DGC.

31 an and experimental mTLE express Reelin, and DGC progenitors express the downstream Reelin signaling

32 M injections both retinal ganglion cells and DGCs were labeled.

33 rentially affects LapA localization, another DGC mainly controls swimming motility, while a third DGC

34 Proteins that contain GGDEF domains act as DGCs, whereas proteins that contain EAL or HD-GYP domain

35 a significant positive relationship between DGC duration and habitat temperature and an important in

36 ntration was significantly different between DGCs, suggesting that bacteria can optimize phenotypic o

37 esult of a sophisticated interaction between DGCs and PDEs.

38 higher DGC activity of the diferrous Vc Bhr-DGC is consistent with induction of biofilm formation in

39 Vc Bhr-DGC showed approximately 10 times higher DGC activity in

40 This protein, Vc Bhr-DGC, was found to contain two tightly bound non-heme iro

41 born DGCs transiently reorganized adult-born DGC local afferent connectivity and promoted global rema

42 DGCs preferentially synapse onto adult-born DGCs after pilocarpine-induced status epilepticus (SE),

43 ture DGCs enhanced integration of adult-born DGCs and increased NSC activation.

44 statin(-) interneuron inputs onto adult-born DGCs are maintained, likely due to preferential sproutin

45 Adult-born DGCs are thought to compete with mature DGCs for inputs

46 jections that specifically target adult-born DGCs arise in the epileptic brain, whereas axons of inte

47 mice with a reduced population of adult-born DGCs at the immature stage were deficient in forming rob

48 mory, yet it remains unknown when adult-born DGCs become involved in the cognitive processes.

49 The survival and activity of the adult-born DGCs can be influenced by the experience of the animal d

50 transiently reduce the numbers of adult-born DGCs in a temporally regulatable manner.

51 he DG by enhancing integration of adult-born DGCs in adulthood, middle age, and aging enhanced memory

52 Enhanced integration of adult-born DGCs transiently reorganized adult-born DGC local affere

53 mature DGCs increased survival of adult-born DGCs without affecting proliferation or DGC activity.

54 The events leading adult-born DGCs' to transition from simple spindle-like morphology

55 d, expanded cohort of age-matched adult-born DGCs.

56 lating the initial integration of adult-born DGCs.SIGNIFICANCE STATEMENT Since the discovery of the c

57 nputs are greatly diminished onto early-born DGCs after SE.

58 Both adult-born and early-born DGCs are targets of new inputs from other DGCs as well a

59 naptic inputs onto adult-born and early-born DGCs in the rat pilocarpine model of mTLE.

60 er their integration differs from early-born DGCs that are mature at the time of epileptogenesis.

61 synapse onto both adult-born and early-born DGCs.

62 re to preferentially synapse onto early-born DGCs.

63 particularly on those proteins bearing both DGC and PDE modules, and for future optimization studies

64 ow-specificity signaling is characterized by DGCs or PDEs that modulate a general signal pool, which,

65 tient diagnosed with diffuse gastric cancer (DGC) before age 50; families with 3 or more cases of DGC

66 (PGC, n = 131) and distal gastric carcinoma (DGC, n = 307) in consecutive 438 EGCs diagnosed with the

67 A1 neuron populations, dentate granule cell (DGC) ensembles activated by learning were not preferenti

68 Dentate granule cell (DGC) neurogenesis persists throughout life in the hippoc

69 Dentate granule cell (DGC) neurogenesis persists throughout life in the mammal

70 h a major focus on the dentate granule cell (DGC) population, to explore the signaling pathways under

71 unctions of adult-born dentate granule cell (DGCs) are poorly understood.

72 retinal input from displaced ganglion cells (DGCs), which are found at the margin of the inner nuclea

73 nputs onto adult-born dentate granule cells (DGCs) are altered in experimental mesial temporal lobe e

74 when adult-generated dentate granule cells (DGCs) are approximately 4 weeks of age, a time point whe

75 New dentate granule cells (DGCs) are continuously generated, and integrate into the

76 pyramidal neurons and dentate granule cells (DGCs) by voltage clamp technique.

77 Adult-born dentate granule cells (DGCs) contribute to learning and memory, yet it remains

78 leptogenesis, adult-generated granule cells (DGCs) form aberrant neuronal connections with neighborin

79 Dentate granule cells (DGCs) have a single, complex, apical dendrite.

80 d newborn hippocampal dentate granule cells (DGCs) in acute mouse brain slices, we found that DA not

81 s of adult-born mouse dentate granule cells (DGCs) in vivo and found that they underwent over-branchi

82 GABA(A) receptors on dentate granule cells (DGCs) is diminished; the molecular mechanism underlying

83 ult-born, hippocampal dentate granule cells (DGCs) is hypothesized to contribute to the development o

84 s by which adult-born dentate granule cells (DGCs) modulate pattern separation to influence resolutio

85 rgic action occurs in dentate granule cells (DGCs), located at the first stage of the hippocampal tri

86 FGF22 on the axons of dentate granule cells (DGCs), which are presynaptic to CA3 pyramidal neurons, i

87 nuous addition of new dentate granule cells (DGCs), which is regulated exquisitely by brain activity,

88 ipal cells of the DG, dentate granule cells (DGCs).

89 into the lumbosacral dorsal gray commissure (DGC) of injured/nontransected rats immediately after inj

90 between the dystrophin-glycoprotein complex (DGC) and laminin in skeletal muscle basal lamina, such t

91 mbly of the dystrophin-glycoprotein complex (DGC) are associated with a spectrum of brain abnormaliti

92 DG) and the dystrophin-glycoprotein complex (DGC) are localized at costameres and neuromuscular junct

93 loss of the dystrophin glycoprotein complex (DGC) from the sarcolemma which contributes to the dystro

94 the entire dystrophin-glycoprotein complex (DGC) from the sarcolemma.

95 The dystrophin-glycoprotein complex (DGC) provides an essential link from the muscle fibre cy

96 The dystrophin-glycoprotein complex (DGC), a multicomponent transmembrane complex linking the

97 mbly of the dystrophin-glycoprotein complex (DGC), and a defective DGC disrupts an essential link bet

98 sembles the dystrophin-glycoprotein complex (DGC), but lacks actin-binding domains.

99 rix via the dystrophin-glycoprotein complex (DGC), exhibit muscular dystrophy, cardiomyopathy, and im

100 within the dystrophin-glycoprotein complex (DGC), is thought to induce myofiber degeneration, althou

101 tion of the dystrophin glycoprotein complex (DGC), which anchors neuronal NOS (nNOS).

102 tion of the dystrophin-glycoprotein complex (DGC).

103 dystrophin-associated glycoprotein complex (DGC).

104 through the dystrophin-glycoprotein complex (DGC).

105 eins of the dystrophin-glycoprotein complex (DGC).

106 dystrophin-associated glycoprotein complex (DGC).

107 - and utrophin (Utr)-glycoprotein complexes (DGC and UGC).

108 corded from DGCs of control animals (control DGCs).

109 furosemide than those recorded from control DGCs.

110 apse in epileptic DGCs compared with control DGCs, in which the subunit was extrasynaptic.

111 nner membrane-localized diguanylate cyclase (DGC) and a known regulator of cellulose biosynthesis.

112 codes two proteins with diguanylate cyclase (DGC) and phosphodiesterase (PDE) domains that modulate t

113 a often encode multiple diguanylate cyclase (DGC) and phosphodiesterase (PDE) enzymes that produce an

114 enes encoding predicted diguanylate cyclase (DGC) and phosphodiesterase proteins (ECA3270 and ECA3271

115 i-GMP is synthesized by diguanylate cyclase (DGC) enzymes and hydrolyzed by phosphodiesterase (PDE) e

116 s inversely governed by diguanylate cyclase (DGC) enzymes and phosphodiesterase (PDE) enzymes, which

117 ovide evidence that the diguanylate cyclase (DGC) GcbA contributes to the regulation of BdlA cleavage

118 ecifically requires the diguanylate cyclase (DGC) SadC, and epistasis analysis indicates that PilY1 f

119 tonic PAO1 requires the diguanylate cyclase (DGC) SadC, previously identified as a regulator of surfa

120 lation of the mRNA of a diguanylate cyclase (DGC), Vca0939; relieving an inhibitory structure in vca0

121 itory site (I-site) of diguanylate cyclases (DGCs) and compared it to the conformation adopted in the

122 -di-GMP is produced by diguanylate cyclases (DGCs) and degraded by phosphodiesterases (PDEs).

123 P metabolism proteins, diguanylate cyclases (DGCs) and phosophodiesterases (PDEs), usually lead to di

124 Opposing activities of diguanylate cyclases (DGCs) and phosphodiesterases (PDEs) control c-di-GMP hom

125 set of genes encoding diguanylate cyclases (DGCs) and phosphodiesterases.

126 di-GMP is catalyzed by diguanylate cyclases (DGCs) containing the GGDEF domain, while its degradation

127 and contains numerous diguanylate cyclases (DGCs) for synthesizing c-di-GMP and phosphodiesterases (

128 Two diguanylate cyclases (DGCs) HmsT and Y3730 (HmsD) are responsible for biofilm

129 n annotation regarding diguanylate cyclases (DGCs) in this bacterium.

130 re predicted to encode diguanylate cyclases (DGCs) or phosphodiesterases (PDEs) were screened for the

131 rmation, with multiple diguanylate cyclases (DGCs) playing distinct roles in these processes, yet lit

132 cteristic of bacterial diguanylate cyclases (DGCs) that catalyze formation of cyclic di-(3',5')-guano

133 -GMP is synthesized by diguanylate cyclases (DGCs) that contain a GGDEF domain and is degraded by pho

134 -GMP is synthesized by diguanylate cyclases (DGCs).

135 The discontinuous gas-exchange cycles (DGCs) observed in many quiescent insects have been a cau

136 e and discovered that loss of SSPN decreased DGC and UGC abundance, leading to impaired laminin-bindi

137 -glycoprotein complex (DGC), and a defective DGC disrupts an essential link between the intracellular

138 nscription factors, PilZ domains, degenerate DGCs or PDEs, and riboswitches.

139 Qrr-dependent DGC activation led to c-di-GMP accumulation and biofilm

140 rives exclusively from aberrantly developing DGCs.

141 These findings indicate that developing DGCs exhibit maturation-dependent vulnerability to SE, i

142 Bacteria typically encode many different DGCs and PDEs within their genomes.

143 Therefore, selecting distinct DGC populations to represent similar but not identical i

144 s can be specifically controlled by distinct DGCs.

145 retroviral (RV) reporters to label dividing DGC progenitors at specific times before or after SE, or

146 In a dual DGC and PDE-A reaction, excess pGpG extends the half-lif

147 ioselective four-dimensional dynamic GC (e4D-DGC) approach to study reversible molecular interconvers

148 Our results demonstrate that hilar ectopic DGCs preferentially synapse onto adult-born DGCs after p

149 ency and (1) the percentage of hilar ectopic DGCs, (2) the amount of mossy fiber sprouting, and (3) t

150 e or after SE decreased MFS or hilar ectopic DGCs, supporting the RV labeling results.

151 In the pilocarpine mTLE model, hilar-ectopic DGCs arise as a result of an aberrant chain migration of

152 spersion and the appearance of hilar-ectopic DGCs.

153 crobes have a large number of genes encoding DGCs and PDEs that are predicted to be part of c-di-GMP

154 soma and dendrites of control and epileptic DGCs was examined with postembedding immunogold electron

155 ed from DGCs of epileptic animals (epileptic DGCs) were less frequent, larger in amplitude, and less

156 of synaptic currents recorded from epileptic DGCs appeared similar to those of recombinant receptors

157 Synaptic currents recorded from epileptic DGCs were less sensitive to diazepam and had altered sen

158 ore commonly within the synapse in epileptic DGCs compared with control DGCs, in which the subunit wa

159 These studies demonstrate that, in epileptic DGCs, the neurosteroid modulation of synaptic currents i

160 ptic marker GAD65 was increased in epileptic DGCs.

161 Finally, optogenetic silencing of existing DGCs during novel environmental exploration perturbed ex

162 P. aeruginosa homolog of the P. fluorescens DGC GcbA involved in promoting biofilm formation via reg

163 lm formation and illustrate a novel role for DGCs in the regulation of the reverse sessile-motile tra

164 raction analysis revealed that at least four DGCs, together with CdgJ, control motility in V. cholera

165 es were observed in recordings obtained from DGCs from refractory SE animals.

166 nanolone modulation than those recorded from DGCs of control animals (control DGCs).

167 Synaptic currents recorded from DGCs of epileptic animals (epileptic DGCs) were less fre

168 ly suggests that YeaJ is indeed a functional DGC.

169 out the potential conservation of functional DGCs across Pseudomonas species.

170 Furthermore, DGCs are unusual in that they are continually generated

171 d (but not 6- or 8-week-old) adult-generated DGCs strongly activated CA3 interneurons.

172 enic mouse model to fate map adult-generated DGCs.

173 f 4-week-old (but not older) adult-generated DGCs.

174 ively delete PTEN from postnatally generated DGCs.

175 gulates rugosity, whereas CdgG does not have DGC activity and negatively regulates rugosity.

176 dition, expression of CdgB or a heterologous DGC in strain KKF457 stimulated F. novicida biofilms, ev

177 The higher DGC activity of the diferrous Vc Bhr-DGC is consistent w

178 Bhr-DGC showed approximately 10 times higher DGC activity in the diferrous than in the diferric form.

179 eriplasmic domain Y3729 (HmsC) inhibits HmsD DGC activity in vitro while an outer membrane Pal-like p

180 During neurogenesis, immature DGCs display distinctive physiological characteristics w

181 These results suggest that immature DGCs that undergo maturation make important contribution

182 strophic or very old animals, disruptions in DGC structure and function impair lateral transmission o

183 strophy nearly identical to that observed in DGC-lacking dystrophic disease models, including a highl

184 s to examine macrophysiological variation in DGC duration in insects.

185 cantly more frequent (32.1%, versus 12.1% in DGCs), as were mucinous and neuroendocrine carcinomas, c

186 nvaded deeper (22.9% into SM2, versus 13% in DGCs), but had fewer (2.9%, versus 16.7% in DGCs) lymph

187 showed shorter (42.4 months, versus 48.3 in DGCs) survival.

188 ly different from those (32.6% and 64.5%) in DGCs.

189 a with lymphoid stroma (6.9%, versus 1.6% in DGCs); but poorly cohesive carcinoma was significantly l

190 DGCs), but had fewer (2.9%, versus 16.7% in DGCs) lymph node metastases.

191 icantly less frequent (5.3%, versus 35.8% in DGCs).

192 smaller (1.9 cm in average, versus 2.2 cm in DGCs), invaded deeper (22.9% into SM2, versus 13% in DGC

193 tion of distinct subtypes of DA receptors in DGCs at different developmental stages.

194 and promote a similar dendrite structure in DGCs.

195 ity signaling is characterized by individual DGCs or PDEs that are specifically associated with downs

196 e decision to fire or not fire by individual DGCs was robust and repeatable at all stages of developm

197 However, individual DGCs showed a significant correlation between c-di-GMP p

198 o track the real-time activity of individual DGCs in freely behaving mice.

199 veloping during SE revealed normally located DGCs exhibiting hilar basal dendrites and mossy fiber sp

200 RV injections 7 weeks before SE to mark DGCs that had matured by the time of SE labeled cells wi

201 nes, Kruppel-like factor 9 (Klf9), in mature DGCs enhanced integration of adult-born DGCs and increas

202 tion by inducible deletion of Rac1 in mature DGCs increased survival of adult-born DGCs without affec

203 Reversal of Klf9 overexpression in mature DGCs restored spines and activity and reset neuronal com

204 st, DA suppressed MPP transmission to mature DGCs to a similar extent but did not influence their LTP

205 born DGCs are thought to compete with mature DGCs for inputs to integrate.

206 These findings suggest that Reelin modulates DGC progenitor migration to maintain normal DGC integrat

207 errant neuronal connections with neighboring DGCs, disrupting the dentate gate.

208 E) stimulates neurogenesis, but many newborn DGCs integrate aberrantly and are hyperexcitable, wherea

209 Eliminating cohorts of newborn DGCs by focal brain irradiation at specific times before

210 We studied establishment of newborn DGCs dendritic pattern and found it was mediated by a si

211 using single-cell transcriptomes of newborn DGCs, and among Golgi-related genes, found the presence

212 igration and aberrant integration of newborn DGCs.

213 animal during a critical period when newborn DGCs are still immature.

214 No DGC- or PDE-encoding protein genes are present in the F.

215 No DGCs were labeled from an injection in the optic tectum.

216 iofilm formation by P. fluorescens Pf0-1, no DGCs from this strain have been characterized to date.

217 DGC progenitor migration to maintain normal DGC integration in the neonatal and adult mammalian dent

218 Treatments that restore normal DGC development after epileptogenic insults may therefor

219 status epilepticus (SE), whereas normotopic DGCs synapse onto both adult-born and early-born DGCs.

220 hey had not been previously exposed, a novel DGC population-rather than the previously activated DGC

221 ore age 50; families with 3 or more cases of DGC; families with 1 DGC before the age of 40; and famil

222 are all fundamental circuit determinants of DGC excitation, critical in both normal and pathological

223 The effects of DGC gene mutations on phenotypes associated with biofilm

224 he age of 40; and families with a history of DGC and lobular breast cancer, with 1 diagnosis before t

225 whether integrin compensates for the loss of DGC and UGC function in SSPN-nulls, we generated mice la

226 e gyrus leads to aberrant chain migration of DGC precursors.

227 frequency-dependent synaptic recruitment of DGC activation in adult, but not developing, animals.

228 nd/or diatomic gas sensing and regulation of DGC activity.

229 iber plasticity, injury-induced sprouting of DGC neurons may be a key constituent in relaying viscera

230 phatase resulted in relocation of the AIS of DGCs without a depolarizing stimulus.

231 ot by alterations in afferent innervation of DGCs because GABA(A) antagonists normalized developmenta

232 The percentage of DGCs, as a proportion of all labeled cells, varied from

233 ion potential firing in large populations of DGCs, we characterized the postnatal development of firi

234 abeled from nBOR, in which the proportion of DGCs was much higher (84-93%).

235 et DGCs discriminating between the I-site of DGCs and the active site of PDEs; this molecule represen

236 nducing proexcitatory changes in a subset of DGCs in isolation is sufficient to cause epilepsy in a r

237 One DGC preferentially affects LapA localization, another DG

238 ecurrent and widespread feedback loops, onto DGCs.

239 born DGCs without affecting proliferation or DGC activity.

240 With the exception of dystrophin, other DGC components were restored to the sarcolemma including

241 pistasis analysis with CdgG, CdgH, and other DGCs and PDEs controlling rugosity revealed that CdgG an

242 rn DGCs are targets of new inputs from other DGCs as well as from CA3 and CA1 pyramidal cells after p

243 of the A-site is also observed in many other DGCs.

244 demonstrate that three of the five predicted DGC genes in E. amylovora (edc genes, for Erwinia diguan

245 ook a systematic mutagenesis of 30 predicted DGCs and found that mutations in just 4 cause reductions

246 tions, deletion of the two biofilm-promoting DGCs increased tissue necrosis in an immature-pear infec

247 Aergic responses in adolescent and adult rat DGCs are still depolarizing from rest.

248 Using a morphologically realistic DGC model, we show that GABAergic action, depending on i

249 pic analysis of the differentially regulated DGCs revealed that a DGC, CdgA, is responsible for the i

250 This selection of a novel responsive DGC population could be triggered by small changes in en

251 To better understand the role DGC neurogenesis plays in seizure-induced plasticity, we

252 se that PilY1 may act via regulation of SadC DGC activity but independently of altering global c-di-G

253 vo c-di-GMP concentration generated by seven DGCs, each expressed at eight different levels, to the c

254 Unlike wild type, a strain lacking all six DGCs did not exhibit a low-temperature-dependent increas

255 Of the 52 mutants tested, deletions of six DGCs and three PDEs were found to affect these phenotype

256 els via expression or activation of specific DGCs.

257 egulatory functions of c-di-GMP-synthesizing DGCs expand beyond surface attachment and biofilm format

258 al small molecule able to selectively target DGCs discriminating between the I-site of DGCs and the a

259 nd for future optimization studies to target DGCs in vivo.

260 ; (ii) the chthonic hypothesis suggests that DGCs facilitate gas exchange during environmental hypoxi

261 he oxidative-damage hypothesis suggests that DGCs minimize oxidative tissue damage.

262 ged: (i) the hygric hypothesis suggests that DGCs reduce respiratory water loss; (ii) the chthonic hy

263 The DGC layer in human and experimental mesial temporal lobe

264 The DGC likely represents a mechanoreceptor in skeletal musc

265 The DGC protects the sarcolemma from contraction-induced inj

266 g the interaction between dystrophin and the DGC and reveal that posttranslational modification of a

267 natal hearts deficient in both Hippo and the DGC showed cardiomyocyte overproliferation at the injury

268 ction between Hippo pathway function and the DGC.

269 In brain, the DGC is involved in the organisation of GABA(A) receptors

270 In the absence of dystrophin, the DGC is disassembled from the sarcolemma.

271 ly, CT alone was sufficient to establish the DGC at the sarcolemma.

272 progress in defining distinct roles for the DGC in neurons and glia.

273 Absence of alpha-syn from the DGC is known to lead to structurally aberrant neuromuscu

274 a model system to investigate if and how the DGC directly regulates the mechanical activation of musc

275 sed membrane residence of the integrins, the DGC/utrophin-glycoprotein complex of proteins and annexi

276 Expression of the DGC and UGC, laminin binding and Akt signaling were nega

277 dystrophin gene disrupt the structure of the DGC causing severe damage to muscle fibres.

278 in which PTEN was deleted from >/= 9% of the DGC population developed spontaneous seizures in about 4

279 , a unique tetraspanin-like component of the DGC, ameliorates muscular dystrophy in dystrophin-defici

280 To examine the functional role of the DGC, we expressed the Dp116 transgene in mice lacking bo

281 o promote the proteasomal degradation of the DGC.

282 effect of synaptically released GABA on the DGC population.

283 gulating HapR, and positively regulating the DGC Vca0939.

284 While R1-3 and R10-12 did not restore the DGC, surprisingly, CT alone was sufficient to establish

285 Here we show that the DGC component dystroglycan 1 (Dag1) directly binds to th

286 These data demonstrate that the DGC is critical for growth and maintenance of muscle mas

287 We conclude that the DGC promotes the mechanical activation of cardiac nNOS b

288 ed laterally from fibre to fibre through the DGC without decrement.

289 < 0.01) c-Fos(+) cell numbers throughout the DGC after injury.

290 o CA3 pyramidal neurons, induces IGF2 in the DGCs.

291 We conclude that the DGCs of insects reduce respiratory water loss while ensu

292 These DGCs were characterized genetically and biochemically to

293 The proportion was small (2-3%), and these DGCs were smaller in size than those projecting to the n

294 increase in c-di-GMP, indicating that these DGCs are required for temperature modulation of c-di-GMP

295 ly controls swimming motility, while a third DGC affects both LapA and motility.

296 IGF2, in turn, localizes to DGC presynaptic terminals and stabilizes them in an acti

297 F. novicida strains lacking either the two DGC/PDE genes (cdgA and cdgB) or the entire gene cluster

298 We previously identified two DGCs, VpvC and CdgA, that can control the switch between

299 nts from retinal ganglion cells, but whether DGCs also project to LM remains unclear.

300 ial perforant path (MPP) inputs to the young DGCs, but also decreased their capacity to express long-