ライフサイエンスコーパス: MAM

1 MAM administration leads to a hyperdopaminergic state co

2 MAM is a peptide mapping method utilizing mass spectrome

3 MAM overproduction and knockout mutants were more and le

4 MAM protein was extracted efficiently by a surfactant-ai

5 MAM-treated male rats were exposed to acute and repeated

6 MAM-treated rats exhibited a heightened level of anxiety

7 li were randomly assigned to provide to 1264 MAM children aged 6-35 mo one of 4 dietary supplements c

8 cks on an acidic surface of the neuropilin-2 MAM domain to polysialylate O-glycans on the adjacent li

9 held in Lorne, Australia, in February 2008 (MAM 2008).

10 ns (with the highest rates in sarcoma [47%], MAM [37%], and NET [32%]), grade 2 in 706 lesions (with

11 Sigma 1 receptor (Sig-1R), a MAM chaperone affecting calcium signaling to mitochondri

12 We demonstrate that VAPB is a MAM protein and that loss of either VAPB or PTPIP51 pert

13 Here, we report the crystal structure of a MAM mutant K201A in apo form (unliganded) at 2.8-A resol

14 Thus, mTORC2 is at the core of a MAM signaling hub that controls growth and metabolism.

15 that received methyl azoxymethanol acetate (MAM) gestationally exhibited higher levels of anxiety pe

16 the mitotoxin methyl azoxymethanol acetate (MAM), we examined the convergent projections from the ve

17 the mitotoxin methyl azoxymethanol acetate (MAM).

18 thylating agent methylazoxymethanol acetate (MAM) at gestational day 17 exhibit as adults behavioral

19 lkylating agent methylazoxymethanol acetate (MAM) on embryonic day 17 (E17) produces behavioral and a

20 biomarkers in a methylazoxymethanol acetate (MAM) rat model of schizophrenia and saline-treated contr

21 The methylazoxymethanol acetate (MAM) rodent model proposes that psychosis develops as a

22 ministration of methylazoxymethanol acetate (MAM) to induce a developmental disruption, which in turn

23 e specifically, methylazoxymethanol acetate (MAM)-treated rats display a decreased density of parvalb

24 ed the prenatal methylazoxymethanol acetate (MAM, E17) exposure model to determine the alterations of

25 ophrenia in the methylozoxymethanol acetate (MAM) rodent model of the disease.

26 results demonstrate that the E. coli adhesin MAM(HS) facilitates retention of a gut commensal by atta

27 In addition, adolescent MAM-treated animals displayed a blunted HPA axis cortico

28 f BLA neurons in both peripubertal and adult MAM rats.

29 Accompanied with this change, adult MAM rats exhibited a significant decrease in spine densi

30 eightened anxiety was also observed in adult MAM animals, as well as higher firing rates of BLA neuro

31 induced increase in BLA theta power in adult MAM rats, supporting a persistent normalization by this

32 revents the hyperdopaminergic state in adult MAM rats.

33 nvestigated the molecular phenotype of adult MAM rats by focusing on the frontal cortex and hippocamp

34 the power of BLA theta oscillations of adult MAM rats showed a larger increase in response to conditi

35 FLT1 inhibition does not affect MAM recruitment to metastatic lesions but regulates a se

36 hildren who sustained recovery for 1 y after MAM treatment.

37 between them, organic molecular amphiphiles (MAMs) and inorganic nanoparticle (NP) amphiphiles (NPAMs

38 this paper we describe the application of an MAM based method for site specific quantification of N-l

39 WH-210, and PB-22, their 5-fluoro analogues (MAM-2201, EAM-2201, and 5F-PB-22, respectively), and the

40 This shows that signal-anchored MAM proteins can make use of hydrophobic interactions in

41 eatic cancer [17%], sarcoma [SAR] [13%], and MAM [8%]), and grade 3 in only 15 lesions.

42 ues in SAR (3.5 +/- 1.8; range, 0.8-2.7) and MAM (3.6 +/- 2.2; range, 0.9-11.6).

43 2 controls StAR processing and activity, and MAM is thus a central location for initiating mitochondr

44 tuating selective sweeps at both the AOP and MAM loci.

45 phic loci controlling GSL variation (AOP and MAM) in natural populations within large blocks of posit

46 ) and that ER-mitochondrial connectivity and MAM function are upregulated in AD We now show that C99,

47 pUL37(COOH) were both detected in the ER and MAM fraction, even though only pUL37(NH2) is preferentia

48 , deoxycholate negatively regulates IcsA and MAM in S. sonnei resulting in reduction in attachment an

49 tation/on-pellet digestion (SOD) method, and MAM proteome was quantified by an ion-current-based MS1

50 nt in purified microsomes, mitochondria, and MAM fractions.

51 d by specific interactions between mucin and MAM(HS) in a sulfation-dependent manner.

52 n limited to analyzing mutations in NICD and MAM.

53 formin improved both insulin sensitivity and MAM integrity.

54 structures of the MAM wild type and another MAM mutant L50A in apo forms at low resolutions.

55 Unexpectedly, the structures of these apo MAM molecules display a three-dimensional domain-swapped

56 was growth factor-stimulated, and mTORC2 at MAM interacted with the IP3 receptor (IP3R)-Grp75-voltag

57 ical studies detected no correlation between MAM production and the severity of arthritis induced in

58 ver and an altered lipid composition of both MAM and mitochondrial membranes.

59 cellular distribution, thus regulating both MAM-specific and plasma membrane proteins.

60 hensive proteome profiling of isolated brain MAM from long-term type 2 diabetic mice vs. non-diabetic

61 tumors (NET; n = 77, 15.3%), mammary cancer (MAM; n = 68, 13.5%), hepatocellular carcinoma (HCC; n =

62 he tears of patients with dry eye, may cause MAM release, allowing rose bengal staining.

63 phology, and surface pattern by coassembling MAMs of block copolymers (BCPs) and NPAMs comprising ino

64 engineered bacterium expressing a commensal MAM on its surface in preventing pathogen attachment and

65 mTORC2 controlled MAM integrity and mitochondrial function via Akt mediate

66 ta) and IL-6 by human myeloma marrow-derived MAMs.

67 mTORC2 deficiency disrupted MAM, causing mitochondrial defects including increases i

68 To dissect MAM activation/cytokine pathways, we analyzed Toll-like

69 TLR4 may cooperate with MHC class II during MAM-induced responses.

70 Dynamic MAM tethering to mitochondria and peroxisomes then coord

71 IA with internal lipid rafts (LRs) in the ER/MAM.

72 d the localization of pUL37x1/vMIA within ER/MAM LRs.

73 Interestingly, only a subset of F2 and F3 MAM rats exhibited increases in dopamine neuron populati

74 To determine the sequences required for MAM importation, we examined pUL37x1 mutants that were p

75 o were enrolled on discharge from an SFP for MAM.

76 lities, might be an alternative strategy for MAM treatment in rural food-secure areas, provided that

77 for NET, HCC, and CCC and lowest values for MAM, CRC, and SAR.

78 re provide evidence that offspring born from MAM-treated rats possess a susceptibility to develop asp

79 e proportion of children that recovered from MAM was significantly higher in the group that received

80 soy/whey RUSF in facilitating recovery from MAM.

81 r overexpression of the mitochondrial fusion/MAM-tethering protein MFN2 nor inhibition/ablation of th

82 ic Grp75, was increasingly enriched in heavy MAM from HCMV-infected cells.

83 getics and calcium homeostasis; however, how MAM is affected under diabetic condition remains elusive

84 However, MAM localization of Bax results in its increased ubiquit

85 from the gut commensal Escherichia coli HS (MAM(HS)), which contains an array of seven mammalian cel

86 ention could be an alternative for improving MAM management.

87 insight into the significant alterations in MAM proteome associated with activation of the UPR in di

88 PFC-evoked responses in control rats, but in MAM-treated rats there was a significant inhibition at s

89 o HLA-DR leads to a conformational change in MAM structure allowing its interaction with TLR2 and TLR

90 In contrast, in MAM-treated rats BLA stimulation increased vHipp-evoked

91 ition of ER with mitochondria, a decrease in MAM function, and an increase in mitochondrial fragmenta

92 alization in endosomes, can also be found in MAM, where it is normally processed rapidly by gamma-sec

93 oncentration of unprocessed C99 increases in MAM regions, resulting in elevated sphingolipid turnover

94 ehavioral expression of latent inhibition in MAM-treated rats.

95 acellular electrophysiological recordings in MAM- and saline-treated rats to evaluate the effect of c

96 loss abrogated the "inflammatory switch" in MAM within nascent myeloma lesions and licensed macropha

97 d the direct involvement of TLR2 and TLR4 in MAM binding and presentation to T cells.

98 .0; range, 0.2-6.3) and the lowest values in MAM (1.7 +/- 0.8; range, 0.2-4.1), CRC (1.8 +/- 0.9; ran

99 ow that CSF1-mediated autocrine signaling in MAMs is downstream of FLT1 and can restore the tumor-pro

100 or TLR4 with HLA-DR significantly increases MAM binding and the subsequent T cell activation compare

101 nylated to measure the efficiency of induced MAM release and surface restoration.

102 e tumor-promoting activity of FLT1-inhibited MAMs.

103 lish that Bax recruitment to the MAM and its MAM-associated degradation (MAMAD) are a newly described

104 We found that juvenile MAM-treated rats emitted significantly more calls, spent

105 Moreover, we found GRP75, a key MAM tethering protein, was drastically reduced by long-t

106 an myeloma-associated monocytes/macrophages (MAM), but not myeloma plasma cells, constitute the predo

107 lation of metastasis-associated macrophages (MAMs) recruited to the lung that promote tumor cell seed

108 t, versikine Myeloma-associated macrophages (MAMs), rather than tumor cells, chiefly produced V1-VCAN

109 rophages, metastasis-associated macrophages (MAMs), which originate from inflammatory monocytes (IMs)

110 on of untreated moderate acute malnutrition (MAM) and severe acute malnutrition (SAM) in children age

111 Children with moderate acute malnutrition (MAM) are often treated with fortified blended flours, mo

112 Children with moderate acute malnutrition (MAM) are treated with lipid-based nutrient supplement (L

113 ho recover from moderate acute malnutrition (MAM) have high rates of relapse in the year after nutrit

114 f children with moderate acute malnutrition (MAM) is based on food supplementation in outpatient prog

115 Management of moderate acute malnutrition (MAM) is, currently, focused on food supplementation appr

116 nt of childhood moderate acute malnutrition (MAM) remains unsettled.

117 Moderate acute malnutrition (MAM), defined as weight-for-length z score between -3 an

118 protein CSL and the coactivator Mastermind (MAM) to up-regulate transcription from Notch target gene

119 parsed using maximal almost-unique matches (MAMs).

120 Rare variants in MDGAs (MAM domain-containing glycosylphosphatidylinositol ancho

121 und in the mitochondria-associated membrane (MAM) fraction, no RAS components could be detected in pu

122 ochondria/mitochondrial-associated membrane (MAM) in the absence of lipid droplet biosynthesis, but a

123 ng is the mitochondrial-associated membrane (MAM), a distinct membrane compartment that links the end

124 hed on the mitochondria-associated membrane (MAM), the site of ER-mitochondria Ca(2+) flux.

125 th the mitochondrion-associated ER membrane (MAM) and mitochondrial proteins.

126 The mitochondria-associated ER membrane (MAM) plays a critical role in cellular energetics and ca

127 termed mitochondria-associated ER membrane (MAM).

128 as the mitochondrion-associated ER membrane (MAM).

129 e., the mitochondria-associated ER membrane (MAM)], they dynamically change the cellular distribution

130 ociated endoplasmic reticulum (ER) membrane (MAM).

131 a-associated endoplasmic reticulum membrane (MAM) prior to its translocation to the mitochondrial mat

132 known as mitochondrion-associated membranes (MAM), and to mitochondria.

133 into the mitochondrion-associated membranes (MAM), the site of contact between the ER and mitochondri

134 calize at mitochondria-associated membranes (MAM), where mitochondria are closely apposed with the en

135 re termed mitochondria-associated membranes (MAM).

136 ciated endoplasmic reticulum (ER) membranes (MAM) and that ER-mitochondrial connectivity and MAM func

137 ciated endoplasmic reticulum (ER) membranes (MAM), a structurally and functionally distinct subdomain

138 through mitochondrion-associated membranes (MAMs) to the outer mitochondrial membrane (OMM), where i

139 vided by mitochondrion-associated membranes (MAMs).

140 to as mitochondria-associated ER membranes (MAMs), and they play an important role in, for example,

141 ned as mitochondria-associated ER membranes (MAMs), which are essential for calcium, lipid and metabo

142 called mitochondria-associated ER membranes (MAMs).

143 own as mitochondria-associated ER membranes (MAMs).

144 ciated endoplasmic reticulum (ER) membranes (MAMs) are functional domains between both organelles inv

145 odels of breast cancer pulmonary metastasis, MAMs uniquely express FLT1.

146 g 4-vinylpiridine (VIPY) and methacrylamide (MAM) as functional monomers, ethylene glycol dimethacryl

147 demonstrated using a multiattribute method (MAM), which can quantify multiple post-translational mod

148 (E17) to the neurotoxin methylazoxymethanol (MAM).

149 efficacy on maleimide-activated microplates (MAM) and gold electrodes.

150 Targeting to mitochondria/MAM and/or the stability of Rdh10 require both the N-ter

151 type 1, which also localizes to mitochondria/MAM before lipid droplet synthesis, and associates with

152 rmacological inhibition of the mitochondrial MAM protein, cyclophilin D (CypD), altered insulin signa

153 The M. arthritidis mitogen (MAM) superantigen has long been implicated as having a r

154 Mycoplasma arthritidis-derived mitogen (MAM) is a member of the superantigen family that structu

155 Mycoplasma arthritidis-derived mitogen (MAM) is a superantigen that can activate large fractions

156 ptors for the multivalent adhesion molecule (MAM) from the gut commensal Escherichia coli HS (MAM(HS)

157 27 which is a multivalent adhesion molecule (MAM) required for invasion of epithelial cells and macro

158 We report a multivalent adhesion molecule (MAM) that enables a wide range of gram-negative pathogen

159 y shown that multivalent adhesion molecules (MAMs) are abundant in both pathogenic and commensal bact

160 sins, termed Multivalent Adhesion Molecules (MAMs) that are essential for initial binding of bacteria

161 The cell-surface molecules, MAM domain-containing glycosylphosphatidylinositol ancho

162 Three membrane-associated mucins (MAMs)--MUC1, MUC4, and MUC16--are expressed at the ocula

163 els of schizophrenia, the neurodevelopmental MAM E17 model and the acute PCP model.

164 ave determined the structure of the CSL-NICD-MAM ternary complex and characterized mutations that aff

165 ese results strongly suggest that binding of MAM to HLA-DR leads to a conformational change in MAM st

166 measures were all higher in visual cortex of MAM rats (posterior hyperactivity), which might parallel

167 The orbitofrontal cortex of MAM rats showed lower resting-state functional magnetic

168 Disruption of MAM integrity by genetic or pharmacological inhibition o

169 We found uniform distribution of MAM in neurons.

170 Regional effects of MAM on the expression of parvalbumin-positive cells (PV)

171 nd (F2) and third (F3) filial generations of MAM-treated rats displays a schizophrenia-like phenotype

172 ltered insulin signaling, the implication of MAM dysfunctions in insulin resistance is unknown.

173 for insulin signaling and that induction of MAM prevented palmitate-induced alterations of insulin s

174 tral role in coordinating the interaction of MAM proteins with the outer mitochondrial membrane trans

175 ebT, the latter of which is an orthologue of MAM-7 that was previously reported to be an outer membra

176 into the MAM, indicating partial overlap of MAM and mitochondrial targeting signals.

177 Perturbation of MAM function has previously been suggested in Alzheimer'

178 A total of 1,313 non-redundant proteins of MAM were identified, among which 144 proteins were found

179 Collectively, our data reveal a new role of MAM integrity in hepatic insulin action and resistance,

180 To study the pathogenic significance of MAM, M. arthritidis mutants that overproduced or failed

181 ++ with 2 RUSF products for the treatment of MAM to test the hypothesis that the recovery rate achiev

182 Whereas supplement-based treatment of MAM was found to be more effective than the provision of

183 portance of milk protein in the treatment of MAM, because the use of a novel whey RUSF resulted in hi

184 f 4 dietary supplements for the treatment of MAM.

185 ined recovery in children after treatment of MAM.

186 her dietary supplements for the treatment of MAM; CSB++ yielded intermediate results.

187 Soluble forms of MAMs are detected in human tears, but the mechanisms of

188 ipid-enriched microdomain (GEM) fractions of MAMs, where it interacts with the phosphorylated form of

189 ng metastasis foci, as well as the number of MAMs accumulated in tumor-challenged lung in mice.

190 obesity leads to a marked reorganization of MAMs resulting in mitochondrial calcium overload, compro

191 are implicated in the release or shedding of MAMs in other epithelia (neutrophil elastase, tumor necr

192 Their grafting on MAM greatly increased the sensitivity of the ELOSA test

193 The enhancing effect of TLR2 or TLR4 on MAM-induced T cell proliferation was not due to TLR liga

194 Mitochondria-associated ER membranes, or MAMs, define the sites of endoplasmic reticulum/mitochon

195 ER; mitochondria-associated ER membranes or 'MAM').

196 Two novel mono(amidine) organocatalysts (MAM) were discovered to provide high levels of enantiose

197 ed ER-mitochondrial apposition and perturbed MAM function lie at the heart of AD pathogenesis.

198 e meprin A5 antigen-mu tyrosine phosphatase (MAM) domain and the O-glycan-containing linker region of

199 Thus, in the prenatal MAM-exposure SZ model, NMDAR expression and function is

200 Mechanistically, Ccr1 deficiency prevents MAM retention in the lung by reducing MAM-cancer cell in

201 tants that overproduced or failed to produce MAM were developed.

202 mparisons indicated that the "reconstituted" MAM monomer from the domain-swapped dimer displays large

203 ion of the CCL2 receptor CCR2, the recruited MAMs secrete another chemokine ligand CCL3.

204 events MAM retention in the lung by reducing MAM-cancer cell interactions.

205 Up-regulated MAM-associated proteins were found in the AD brain and a

206 thelial cell line (HCLE) expressing the same MAMs as native tissue was used.

207 The ER-mitochondrial contact site (MAM) is essential for fission of mitochondria prior to e

208 The S. sonnei MAM mediates intimate attachment to host cells, which is

209 In behavioral studies, MAM (vs. SHAM) rats displayed abnormal orbitofrontal cor

210 e of the Mycoplasma arthritidis superantigen MAM.

211 hysiologic agents that induce ocular surface MAM release.

212 Thus, targeting MAM-based adherence is a promising strategy for displaci

213 not clear; however, we now demonstrate that MAM induces differential DNA methylation, which may be h

214 Our results demonstrate that MAM quantification of individual glycan species from bot

215 We demonstrated that MAM integrity is required for insulin signaling and that

216 Interestingly, we also found that MAM complexed with soluble HLA-DR is capable of binding

217 We found that MAM-exposed animals have significantly altered NMDAR pro

218 We have found that MAM-localized functions are increased significantly in c

219 Further comparison indicated that MAM has a flexible N-terminal loop, implying that confor

220 This has lead to the premise that MAM rats are a neurodevelopmental model for schizophreni

221 We now show that MAM function and ER-mitochondrial communication-as measu

222 We also show that MAM is an intracellular detergent-resistant lipid raft (

223 Our results showed that MAM fails to bind to TLR2- and TLR4-transfected cells.

224 The MAM region of the ER is a lipid raft-like domain closely

225 The MAM(HS) adhesin interacted with a range of host receptor

226 The MAM, which is highly capable of accumulating ceramides,

227 The MAM, which serves as a site for lipid transfer and calci

228 hat determines the location of Sig-1R at the MAM and how the receptor translocation is initiated is u

229 FUNDC1 accumulates at the MAM by associating with the ER membrane protein calnexin

230 C1/IP3R1 and Grp75/IP3R1 interactions at the MAM interface.

231 mitochondria are physically connected at the MAM.

232 the pathogenesis of Alzheimer's disease: the MAM hypothesis.

233 rotein, pUL37x1, trafficked into the ER, the MAM, and the mitochondria.

234 sable genes included the gene coding for the MAM superantigen and genes coding for ribosomal proteins

235 and causes translocation of Sig-1R from the MAM to ER cisternae.

236 nvolve the translocation of Sig-1Rs from the MAM to other parts of the cell, whereby Sig-1Rs bind and

237 ge differences at the hinge regions from the MAM(wt) molecule in the receptor-bound form.

238 s this synapse for MAVS proteolysis from the MAM, but not from mitochondria, to ablate RIG-I signalin

239 attenuated reversal learning deficits in the MAM but not acute PCP model.

240 ignaling to mitochondria, is anchored in the MAM by its LR association.

241 of PV and mGlu5 expression was found in the MAM model in several regions of importance in schizophre

242 onstrate abnormal stress responsivity in the MAM model of schizophrenia and suggest that these animal

243 t mesolimbic dopamine neuron function in the MAM model of schizophrenia.

244 nd neuroendocrine responses to stress in the MAM model of schizophrenia.

245 tem function and associated behaviors in the MAM model.

246 s not due to TLR ligand contamination in the MAM preparation.

247 ed with PCP to resemble that observed in the MAM rat.

248 In the MAM, StAR interacts with mitochondrial proteins Tom22 an

249 omologue localizes almost exclusively in the MAM.

250 with intracellular membranes, including the MAM, through membrane-targeting domains within NS4A and

251 protein, HCMV pUL37x1, trafficking into the MAM during permissive infection and HCMV-induced alterat

252 signal were reduced in trafficking into the MAM, indicating partial overlap of MAM and mitochondrial

253 V UL37 proteins traffic from the ER into the MAM, where they are sorted into either the secretory pat

254 tion via Akt mediated phosphorylation of the MAM associated proteins IP3R, Hexokinase 2, and phosphof

255 ission and mitophagy at the interface of the MAM by working in concert with DRP1 and calnexin under h

256 Surprisingly, a component of the MAM calcium signaling junction complex, cytosolic Grp75,

257 ecific acidic residues on the surface of the MAM domain are critical for neuropilin-2 polysialylation

258 infection and HCMV-induced alteration of the MAM protein composition.

259 tially refined the crystal structures of the MAM wild type and another MAM mutant L50A in apo forms a

260 Our work demonstrates that the MAM method is a suitable approach for providing quantita

261 mic and metabonomic analyses showed that the MAM treatment on E17 resulted primarily in deficits in h

262 These findings suggest that the MAM, bearing cholesterol and ceramide-enriched microdoma

263 ombined with functional validation, that the MAM-E17 rat model reproduces hippocampal deficits releva

264 Because of its trafficking through the MAM and partial colocalization with Sig-1R, we tested wh

265 Thus, the MAM mediates an intracellular immune synapse that direct

266 esults establish that Bax recruitment to the MAM and its MAM-associated degradation (MAMAD) are a new

267 te that wild-type alpha-syn localizes to the MAM and modulates mitochondrial morphology, and that the

268 we establish that vMIA retargets Bax to the MAM as well as to the OMM from immediate early through l

269 A virus infection, RIG-I is recruited to the MAM to bind MAVS.

270 DRP1 is thereby recruited to the MAM, and mitochondrial fission then occurs.

271 n important role in anchoring Sig-1Rs to the MAM.

272 in motif and palmitoylation to target to the MAM.

273 nce did not affect StAR association with the MAM and thus its mitochondrial targeting.

274 hese studies are broadly consistent with the MAM model, caution is required when comparing data acros

275 evant signaling pathways associated with the MAM proteome changes in diabetes, most significantly the

276 The entire C-terminal domains of these MAM molecules are involved in the domain swapping.

277 mTORC2 localization to MAM was growth factor-stimulated, and mTORC2 at MAM inte

278 o-use supplementary food (RUSF), in treating MAM through first-line rural health services.

279 hosphate is completely released from Gd-TREN-MAM below pH 2.

280 In water at neutral pH, Gd-TREN-MAM binds phosphate with high affinity (Ka = 1.3 x 10(4)

281 even under strong acidic conditions, Gd-TREN-MAM can be used at least 10 times in a pH-based recyclin

282 Gd-TREN-MAM is highly selective for phosphate over other anions

283 onyl))tris(4-ox o-4H-pyran-3-olate) (Gd-TREN-MAM).

284 r sorting protein-2 and sigma1 receptor, two MAM-associated proteins, were shown to be essential for

285 The duration of untreated MAM appears to have been shorter among children aged 6-3

286 hood estimates for the duration of untreated MAM, defined by weight-for-height z score and middle upp

287 We propose that upregulated MAM function at the ER-mitochondrial interface, and incr

288 The upregulated MAM binding and activity in HLA-DR/TLR-transfected cells

289 The mechanisms by which MAM produces this phenotype are not clear; however, we n

290 Sig-1Rs associate with MAM-derived DRMs but not with those from microsomes.

291 tested whether pUL37x1/vMIA associates with MAM LRs.

292 While Bax association with MAM lipid rafts was detected in HCMV-infected cells, ass

293 a-syn result in its reduced association with MAM, coincident with a lower degree of apposition of ER

294 l recruited 6- to 23-month-old children with MAM in Burkina Faso.

295 ine the treatment effect among children with MAM included by MUAC and aged >/=6 mo with lengths <67 c

296 Based on this study, children with MAM mainly gain fat-free tissue when rehabilitated.

297 oncentrate in the treatment of children with MAM. kg(-1) . d(-1) for up to 12 wk.

298 iation of Bax and apoptosome components with MAM lipid rafts.

299 mpairments were qualitatively distinct, with MAM increasing perseverative responding, whereas the PCP

300 pe that overlaps the region of identity with MAM, significantly inhibited these activities when trigg

301 not enter the mitochondria or interact with MAM-associated proteins, and therefore steroidogenesis w