ライフサイエンスコーパス: mitochondrial fusion

1 d interaction of MYO2 and genes required for mitochondrial fusion.

2 otypes are not necessarily caused by altered mitochondrial fusion.

3 association, which is a necessary prelude to mitochondrial fusion.

4 levels of Fzo1 and maintenance of efficient mitochondrial fusion.

5 on is necessary for increased IHG-1-mediated mitochondrial fusion.

6 , a molecule required for maintaining proper mitochondrial fusion.

7 h long and short forms of OPA1 and maintains mitochondrial fusion.

8 of YAP2 in human cell lines causes increased mitochondrial fusion.

9 morphology and have overlapping functions in mitochondrial fusion.

10 gulates the lipid and protein machineries of mitochondrial fusion.

11 phosphorylation sites, leading to unopposed mitochondrial fusion.

12 Further, MODE 2 sequestration prevents mitochondrial fusion.

13 ondrial transport, distinct from its role in mitochondrial fusion.

14 ic animals is also associated with depressed mitochondrial fusion.

15 een Fzo1 GTP hydrolysis, ubiquitylation, and mitochondrial fusion.

16 FZO-1 is important for its ability to cause mitochondrial fusion.

17 hosphatases Mfn1,2 and Opa1 are required for mitochondrial fusion.

18 nduction of mitochondrial beta-oxidation and mitochondrial fusion.

19 optic atrophy 1 (OPA1), the key proteins for mitochondrial fusion.

20 ity in cells that regulates apoptosis and/or mitochondrial fusion.

21 In yeast, three proteins are essential for mitochondrial fusion.

22 ropathy, result from a primary deficiency of mitochondrial fusion.

23 on and enhanced by perturbations that reduce mitochondrial fusion.

24 e levels of Fzo1p are required for efficient mitochondrial fusion.

25 zo1p degradation in the multistep process of mitochondrial fusion.

26 between the two mitofusins in the control of mitochondrial fusion.

27 odel for neurodegeneration caused by loss of mitochondrial fusion.

28 y Mfn2 disease mutants are nonfunctional for mitochondrial fusion.

29 itochondrial membrane, which plays a role in mitochondrial fusion.

30 of neurodegeneration due to perturbations in mitochondrial fusion.

31 or the dependence of respiratory activity on mitochondrial fusion.

32 how individual OPA1 splice forms function in mitochondrial fusion.

33 tofusin 2 (Mfn2) and that may participate in mitochondrial fusion.

34 about how these domains interact to mediate mitochondrial fusion.

35 lipid-modifying enzymes that is required for mitochondrial fusion.

36 d caused increased fragmentation by blocking mitochondrial fusion.

37 1p and thereby link these two GTPases during mitochondrial fusion.

38 proteins form protein complexes that mediate mitochondrial fusion.

39 in-related Mgm1 protein is also required for mitochondrial fusion.

40 determine to be due to a severe reduction in mitochondrial fusion.

41 the GTPase domain of Mgm1p completely block mitochondrial fusion.

42 hree separate molecular complexes to promote mitochondrial fusion.

43 duced oxidative phosphorylation and enhanced mitochondrial fusion.

44 ) as new Smad2 binding partners required for mitochondrial fusion.

45 namin-related GTPases that are essential for mitochondrial fusion.

46 mportant and elusive process of MFN-mediated mitochondrial fusion.

47 bc13 inactivation abrogates parkin-dependent mitochondrial fusion.

48 ion, suppressing mitophagy without impairing mitochondrial fusion.

49 al respiratory capacity, ATP production, and mitochondrial fusion.

50 quitin ligases Mdm30 and Rsp5 that modulates mitochondrial fusion.

51 omes, chloroplasts, and endosomes [1] and in mitochondrial fusion [2].

52 e or more short isoforms support substantial mitochondrial fusion activity.

53 Drp1 activity and shifts the balance toward mitochondrial fusion, adding another layer of complexity

54 ystems has shown that Mfn-2 is a mediator of mitochondrial fusion, an evolutionarily conserved proces

55 l insights into the molecular events driving mitochondrial fusion and advance our understanding of th

56 , overexpression of IHG-1 leads to increased mitochondrial fusion and also protects cells from reacti

57 N2 (the gene encoding mitofusin 2) interrupt mitochondrial fusion and cause the untreatable neurodege

58 SPRY2 KD cells displayed impaired mitochondrial fusion and cell membrane damage, explainin

59 Mitochondrial fusion and division play important roles i

60 oteins Fzo1 and Dnm1, which are required for mitochondrial fusion and division, respectively.

61 Ablation of the mitochondrial fusion and endoplasmic reticulum (ER)-teth

62 Here, we examined mitochondrial fusion and energetic activities in cells p

63 t the differential roles of L- and S-OPA1 in mitochondrial fusion and energetics are ill-defined.

64 tions in Mfn1 or Mfn2 retained low levels of mitochondrial fusion and escaped major cellular dysfunct

65 Mitochondrial fusion and fission affect the distribution

66 Mitochondrial fusion and fission appear essential for he

67 Because of these important functions, mitochondrial fusion and fission are essential in mammal

68 Mitochondrial fusion and fission are mediated by several

69 on the intimate relationship between normal mitochondrial fusion and fission balances, as influenced

70 the first time that retuning the balance of mitochondrial fusion and fission can restore tissue inte

71 Surprisingly, cells deficient in mitochondrial fusion and fission distributed and inherit

72 PLD6 alters mitochondrial fusion and fission dynamics downstream of

73 Disturbed mitochondrial fusion and fission have been linked to var

74 In this article, we investigate beta-cell mitochondrial fusion and fission in detail and report al

75 ROS also shift the balance between mitochondrial fusion and fission in favor of increased f

76 eplication, thus revealing crucial roles for mitochondrial fusion and fission in maintaining the inte

77 Some of the major molecules mediating mitochondrial fusion and fission in mammals have been di

78 ing the mechanisms underlying the control of mitochondrial fusion and fission is critical to understa

79 is a novel regulatory factor controlling the mitochondrial fusion and fission machinery.

80 These data suggest that alterations in mitochondrial fusion and fission play a critical role in

81 proteins have been implicated in controlling mitochondrial fusion and fission processes in both livin

82 nd mtDNA depletion as well as aberrations of mitochondrial fusion and fission proteins, which eventua

83 We will address the ability of mitochondrial fusion and fission to impact all cell type

84 Although mitochondrial fusion and fission were dispensable for mt

85 alterations of the opposing forces governing mitochondrial fusion and fission, similarly affect retin

86 of BCL2-like proteins may be as couplers of mitochondrial fusion and fission.

87 east, flies, and mammals are known to affect mitochondrial fusion and function.

88 on of mitofusin via HUWE1, thereby promoting mitochondrial fusion and function.

89 es mitofusin 2 (Mfn2), a protein involved in mitochondrial fusion and in tethering of mitochondria to

90 Thus, OMM protein distribution depends on mitochondrial fusion and is a locus of apoptotic dysfunc

91 two mammalian mitofusin GTPases that promote mitochondrial fusion and maintain organelle integrity.

92 (OPA1), a dynamin-like GTPase that regulates mitochondrial fusion and maintenance of cristae architec

93 codes a dynamin-related GTPase implicated in mitochondrial fusion and maintenance of the mitochondria

94 s partially rescued by mutants that regulate mitochondrial fusion and maintenance of the tubular morp

95 results shed light on the molecular basis of mitochondrial fusion and mitofusin-related human neuromu

96 two opposing processes: bud-tip anchorage by mitochondrial fusion and Mmr1p, which favors bulk inheri

97 uced OMA1 activation and OPA1 cleavage limit mitochondrial fusion and promote neuronal death.

98 related to human SLP2, a protein involved in mitochondrial fusion and protein complex formation in th

99 These findings reveal that although mitochondrial fusion and regulated exocytic fusion are m

100 These inhibitors also suppress mitochondrial fusion and respiratory defects in IBMPFD p

101 control levels attenuated the htau-enhanced mitochondrial fusion and restored the functions, while d

102 Disruption of OPA1 by RNAi also blocked all mitochondrial fusion and resulted in similar cellular de

103 lacking both Mfn1 and Mfn2 completely lacked mitochondrial fusion and showed severe cellular defects,

104 Mitochondrial fusion and structure depend on the dynamin

105 ains are required for its ability to promote mitochondrial fusion and that Mgm1p self-interacts, sugg

106 sociated regulatory factor), is required for mitochondrial fusion and transport in long axons.

107 ase associated MFN2 proteins suppressed both mitochondrial fusion and transport, and produced classic

108 nnection, mitofusin 2 (Mfn2) participates in mitochondrial fusion and undergoes repression in muscle

109 tic vesicle cycling, glutamate transmission, mitochondrial fusion, and calcium buffering, is complex

110 ndrial permeability transition pore (mtPTP), mitochondrial fusion, and mtDNA biogenesis have already

111 The chronic inhibition of mitochondrial fusion as a result of genetic mutation is

112 an impaired mRNA export is not dependent on mitochondrial fusion, as the deletion of FZO1, an essent

113 By combining an in vitro mitochondrial fusion assay with electron cryo-tomography

114 Using a mitochondrial fusion assay, we established that L-OPA1 c

115 rane fusion DRPs using an in vitro mammalian mitochondrial fusion assay.

116 e results highlight the importance of normal mitochondrial fusion balance, as influenced by the OPA1

117 This observation suggests a requirement for mitochondrial fusion, beyond maintenance of organelle mo

118 ls of fission genes, and increased levels of mitochondrial fusion, biogenesis and synaptic genes in S

119 optotic effect is independent of its role in mitochondrial fusion but mainly mediated by inhibition o

120 phatidylethanolamine is proposed to regulate mitochondrial fusion, but its mechanism of action is unk

121 Bax seems to induce mitochondrial fusion by activating assembly of the large

122 that the Mdm30-Ubp2-Rsp5 crosstalk regulates mitochondrial fusion by coordinating an intricate balanc

123 ammalian Phospholipase D MitoPLD facilitates mitochondrial fusion by generating the signaling lipid p

124 elegans has previously been shown to promote mitochondrial fusion by physically interacting with the

125 inactive cytoplasmic Smad2 rapidly promotes mitochondrial fusion by recruiting RIN1 into a complex w

126 demonstrate that mitochondrial PE regulates mitochondrial fusion by regulating the biophysical prope

127 ns, and demonstrate that mitofusin-dependent mitochondrial fusion can be regulated in mouse cells by

128 Interruption of mitochondrial fusion causes lethal cardiac failure at a

129 1 to mitochondria , as well as to a block in mitochondrial fusion , cellular mechanisms underlying th

130 amic balance between the opposing actions of mitochondrial fusion, controlled by Mitofusin (mfn) and

131 This suggests that the mitochondrial fusion defect in the Deltapsd1 strain coul

132 tochondrial fusion, further exacerbating the mitochondrial fusion defect of the Deltapsd1 strain.

133 s interconnected mitochondrial network and a mitochondrial fusion defect that is not explained by alt

134 ecies are key mediators of cardiomyopathy in mitochondrial fusion-defective cardiomyocytes.

135 Model and analyze mitochondrial fusion defects in Drosophila melanogaster

136 Surprisingly, a defect in maternal mitochondrial fusion delays PME, which is reversed by a

137 the deletion of FZO1, an essential gene for mitochondrial fusion, does not alter the export of ADH1,

138 ed and aggregated mitochondria with impaired mitochondrial fusion during mating.

139 fission in Deltamgm1 cells fails to restore mitochondrial fusion during mating.

140 lated by cytoplasmic lipases, autophagy, and mitochondrial fusion dynamics, ensuring maximum oxidativ

141 In addition, mitochondrial fusion/dynamics were compromised in Ptpmt1

142 smic reticulum (ER) shape in addition to its mitochondrial fusion effects.

143 udies reveal that Mfn1, a GTPase involved in mitochondrial fusion, establishes a mitochondrial size t

144 he mitochondrial ATP pool via a shift toward mitochondrial fusion, excess mitochondrial reactive oxyg

145 otic Bcl2 protein, Bax, positively regulates mitochondrial fusion exclusively through homotypic MFN2

146 ondrial assembly regulatory factor (Marf), a mitochondrial fusion factor (mitofusin), as well as othe

147 ssociated Gp78 ubiquitin ligase and the Mfn1 mitochondrial fusion factor in mitophagy.

148 dependent degradation of the mitofusin (Mfn) mitochondrial fusion factors Mfn1/Mfn2.

149 48 h in Caenorhabditis elegans, and requires mitochondrial fusion, fission and autophagy, providing g

150 'Mitochondrial dynamics', the processes of mitochondrial fusion, fission, biogenesis and mitophagy

151 chondrial dysfunction with marked changes in mitochondrial fusion, fission, morphology and transcript

152 discuss the reciprocal interactions between mitochondrial fusion, fission, transport and mitophagy.

153 l dynamics, incorporating recent findings on mitochondrial fusion, fission, transport and mitophagy.

154 Mitochondrial fusion-fission cycles ensure independent g

155 bscured details of morphological dynamics of mitochondrial fusion/fission and ER remodeling, as well

156 on-defective mitochondrial size decreases, a mitochondrial fusion/fission cycle in adult mouse hearts

157 re interactions between pink1/parkin and the mitochondrial fusion/fission machinery.

158 ng that alpha-syn operates downstream of the mitochondrial fusion/fission machinery.

159 In contrast, key players in mitochondrial fusion/fission or biogenesis were not sign

160 Here, we review newly described functions of mitochondrial fusion/fission proteins in cardiac mitocho

161 pro-fusion effect by increasing the ratio of mitochondrial fusion/fission proteins without resulting

162 arance of damaged mitochondria by autophagy, mitochondrial fusion/fission, and biogenesis) may contri

163 in organelle division, viral resistance, and mitochondrial fusion/fission.

164 iogenesis of s-Mgm1, a protein essential for mitochondrial fusion, further exacerbating the mitochond

165 Remarkably, concomitant deletion of the mitochondrial fusion gene Mfn1 completely rescued heart

166 Mutations in the mitochondrial fusion gene Mfn2 cause the human neurodege

167 Increased synaptic and mitochondrial fusion genes and decreased fission genes w

168 (fission 1) and decreased expression of the mitochondrial fusion genes Mfn1 (mitofusin 1), Mfn2 (mit

169 cently emerged, implicating mutations in the mitochondrial fusion genes OPA1 and MFN2 in the pathogen

170 ommonly caused by mutations in the canonical mitochondrial fusion genes OPA1 and MFN2, respectively.

171 Mitochondrial fusion has not been observed in postmitoti

172 Cells deficient in mitochondrial fusion have been shown to have defects lin

173 i) verapamil suppressed both contraction and mitochondrial fusion, (ii) after spontaneous contraction

174 ochondrial fission and rescued by decreasing mitochondrial fusion, implying that mitochondria can phy

175 Mitochondrial fusion in adult cardiac myocytes is necess

176 that mutant SOD1 motor neurons have impaired mitochondrial fusion in axons and cell bodies.

177 Both forms of Bax restore mitochondrial fusion in Bax/Bak-null cells, which otherw

178 Here we report a role for mitochondrial fusion in bud-tip anchorage of mitochondri

179 rs describe how insulin signalling regulates mitochondrial fusion in C. elegans, and show that mitoch

180 SCF(LIN-23)-regulated pathway that controls mitochondrial fusion in Caenorhabditis elegans by repres

181 e BCL-2-like protein CED-9 in the control of mitochondrial fusion in Caenorhabditis elegans.

182 Here we examine the functions of mitochondrial fusion in differentiated skeletal muscle t

183 dvance our understanding of the evolution of mitochondrial fusion in eukaryotic cells.

184 The role of mitochondrial fusion in functioning of the heart, where

185 in breast cancer, is a pivotal regulator of mitochondrial fusion in glucose-starved cancer cells.

186 to promptly restore cellular metabolism and mitochondrial fusion in keeping with the short residence

187 ndrial membrane protein that participates in mitochondrial fusion in mammalian cells, contributes to

188 ts, blocking DNM1-dependent fission restores mitochondrial fusion in mgm1ts cells during mating.

189 Suppressing cardiomyocyte mitochondrial fusion in Parkin-deficient fly heart tubes

190 ochondrial biogenesis in patient muscle, and mitochondrial fusion in patient fibroblasts associated w

191 Visualizing mitochondrial fusion in real time, we identified two cla

192 This pathway is required for mitochondrial fusion in response to physical exertion, a

193 rough FZO-1/Mfn1,2 and EAT-3/Opa1 to promote mitochondrial fusion in response to specific cellular si

194 ll identify how diet-dependent modulation of mitochondrial fusion in specific neuronal circuits impac

195 morphology, demonstrating a central role for mitochondrial fusion in the cardiomyopathy provoked by i

196 al ATP production in POMC neurons, promoting mitochondrial fusion in their neurites, and increasing P

197 Long OPA1 forms were sufficient to mediate mitochondrial fusion in these cells.

198 d organ function of disrupting cardiomyocyte mitochondrial fusion in vivo.

199 with increased C18:0 dietary intake boosting mitochondrial fusion in vivo.

200 s not yet been possible to directly modulate mitochondrial fusion, in part because the structural bas

201 Suppressing mitochondrial fusion increased compensatory expression o

202 ent increased Opa-1 protein levels, promoted mitochondrial fusion, increased mitochondrial membrane p

203 wever, mgm1 dnm1 mutants remain defective in mitochondrial fusion, indicating that mitochondrial fusi

204 Thus, mitochondrial fusion is an essential and direct target o

205 During apoptosis, mitochondrial fusion is blocked independently of caspase

206 These cellular observations may explain why mitochondrial fusion is essential for embryonic developm

207 Therefore, mitochondrial fusion is essential for embryonic developm

208 The increased mitochondrial fusion is essential for longevity in the d

209 Mitochondrial fusion is essential for maintenance of mit

210 Mitochondrial fusion is essential to cardiomyocyte mitoc

211 When mitochondrial fusion is genetically attenuated, the York

212 Mitochondrial fusion is less well understood but distinc

213 ing mtDNA function in the face of mutations, mitochondrial fusion is likely to be a protective factor

214 animals and yeasts, in which CL's effect on mitochondrial fusion is more profound, Arabidopsis CL pl

215 hondrial fusion in C. elegans, and show that mitochondrial fusion is necessary, but not sufficient, f

216 Our results suggest that increased mitochondrial fusion is not a major driver of longevity,

217 CED-9-induced mitochondrial fusion is not required for the maintenance

218 howed that key cellular functions decline as mitochondrial fusion is progressively abrogated.

219 t, in which mitochondrial fission occurs but mitochondrial fusion is restricted, suggesting that ced-

220 Mitochondrial fusion is thought to be important for supp

221 ns Mfn1 and Mfn2, large GTPases that mediate mitochondrial fusion, is induced by Parkin upon membrane

222 igomeric mitochondrial protein important for mitochondrial fusion, is mutated in Charcot-Marie-Tooth

223 hondria from diverse eukaryotes, followed by mitochondrial fusion (limited mechanistically to green p

224 Formation of lamellar cristae depends on the mitochondrial fusion machinery through a pathway that is

225 ion of Opa-1 and mitofusins, proteins of the mitochondrial fusion machinery, is dramatically altered

226 hosphorylation-stimulated degradation of the mitochondrial fusion machinery.

227 er membrane protein Ugo1, a component of the mitochondrial fusion machinery.

228 ion phenotype, neither overexpression of the mitochondrial fusion/MAM-tethering protein MFN2 nor inhi

229 Interfering with mitochondrial fusion mechanisms in Agrp neurons by cell-

230 discover new proteins that interact with the mitochondrial fusion mediator mitofusin 2 (Mfn2) and tha

231 The expression of genes involved in mitochondrial fusion (Mfn1, Opa1) and fission (Drp1, Fis

232 Thus, attenuated mitochondrial fusion might contribute to the pathogenesi

233 HG-1 forms complexes with known mediators of mitochondrial fusion-mitofusins (Mfns) 1 and 2-and enhan

234 phology observed in a drp-1 mutant, in which mitochondrial fusion occurs but mitochondrial fission is

235 Mitochondrial fusion occurs in many eukaryotes, includin

236 The block in mitochondrial fusion occurs within the same time range a

237 demonstrate that CED-9 can promote complete mitochondrial fusion of both the outer and inner mitocho

238 To directly test the effect of reduced mitochondrial fusion on hepatic metabolism, we generated

239 lished role of mitofusins (MFN1 and MFN2) in mitochondrial fusion, only MFN2 has been associated with

240 a within migrating cells by interfering with mitochondrial fusion (opa-1) or fission (drp-1) proteins

241 hrough a mechanism that depends on increased mitochondrial fusion, Opa-1, and the Akt-mTOR-NFkappaB p

242 cells was not associated with inhibition of mitochondrial fusion or bioenergetic defects, supporting

243 ivo mouse models in which mitofusin-mediated mitochondrial fusion or dynamin-related protein 1-mediat

244 Defects in mitochondrial fusion or fission are associated with many

245 several disease models, the manipulation of mitochondrial fusion or fission can partially rescue dis

246 cellular context, BCL2-like proteins promote mitochondrial fusion or fission.

247 n of Fzo1p have both been shown to alter the mitochondrial fusion process indicating that maintenance

248 d in this process, one of which includes the mitochondrial fusion promoting GTPase Fzo1.

249 We show that the mitochondrial fusion-promoting factor Drosophila Mitofus

250 p97 acts by targeting the mitochondrial fusion-promoting factor mitofusin for degr

251 ous loss-of-function mutations affecting the mitochondrial fusion-promoting factors OPA1 and Mfn2.

252 her levels of total and active Drp1 and less mitochondrial fusion protein 1 (Mfn1).

253 al fusion by physically interacting with the mitochondrial fusion protein FZO-1.

254 ich mutations in this ubiquitously expressed mitochondrial fusion protein lead to neuropathy has not

255 ndrial fission activity or inhibition of the mitochondrial fusion protein Marf-1 in posterior-localiz

256 Mutations in the mitochondrial fusion protein mitofusin 2 (MFN2) are the

257 Importantly, co-expression of mitochondrial fusion protein mitofusin 2 (Mfn2) could ab

258 Elimination of the mitochondrial fusion protein mitofusin 2 (Mfn2) sensitiz

259 monstrates that a phosphorylated form of the mitochondrial fusion protein Mitofusin 2 serves as a rec

260 Here, we examine the role of the mitochondrial fusion protein optic atrophy 1 (OPA1) in d

261 Here we report that OPA1, a mitochondrial fusion protein, was hyperacetylated in hea

262 f lipid mixing and the biogenesis of Mgm1, a mitochondrial fusion protein.

263 mitochondrial trafficking adaptors, and the mitochondrial fusion proteins (mitofusins).

264 se that induces degradation of the mitofusin mitochondrial fusion proteins and mitochondrial fission.

265 Mitochondrial fusion proteins attenuate apoptosis by inh

266 experiments indicate a fundamental role for mitochondrial fusion proteins in mammalian physiology.

267 Despite normal or increased levels of mitochondrial fusion proteins in mtPE-deficient cells, a

268 Transfection of HL-1 cells with the mitochondrial fusion proteins mitofusin 1 or 2 or with D

269 Bak interacts with Mfn1 and Mfn2, two mitochondrial fusion proteins.

270 e resulting OPA1 depletion causes a block in mitochondrial fusion, providing a compelling mechanism f

271 sing this assay, we visualize and quantitate mitochondrial fusion rates in healthy and apoptotic cell

272 he diverse longevity pathways, as inhibiting mitochondrial fusion reduces their lifespans to wild-typ

273 nd significantly decreased expression of the mitochondrial fusion related protein MFN1.

274 sturbances in mitochondrial architecture and mitochondrial fusion-related genes are observed in situa

275 ever, the mechanism by which lipids regulate mitochondrial fusion remains poorly understood.

276 In Saccharomyces cerevisiae, mitochondrial fusion requires at least two outer membran

277 ive in mitochondrial fusion, indicating that mitochondrial fusion requires Mgm1p regardless of the mo

278 Mitochondrial fusion requires the coordinated fusion of

279 Mitochondrial fusion requires two integral outer membran

280 In yeast, mitochondrial fusion requires Ugo1p and two GTPases, Fzo

281 Perturbation of mitochondrial fusion results in defects in mitochondrial

282 tively controls mRNA export independently of mitochondrial fusion, revealing a novel function of an F

283 lated experiment, we find that disruption of mitochondrial fusion strongly increases mitochondrial dy

284 ptional up-regulation of genes that regulate mitochondrial fusion, such as opa1-like (opa1) and mitoc

285 In fibroblasts lacking mitochondrial fusion, the majority of mitochondria lack

286 m reveals a central mechanism that regulates mitochondrial fusion, the manipulation of which can corr

287 e GTPase domains of Fzo1p and Mgm1p regulate mitochondrial fusion, they were not required for associa

288 lian cells have multiple pathways to control mitochondrial fusion through regulation of the spectrum

289 on GTPase dynamin-related protein 1 promoted mitochondrial fusion, thus coupling mitochondrial energe

290 ian cells were corrected upon restoration of mitochondrial fusion, unlike the irreversible defects fo

291 In contrast, disruption of mitochondrial fusion via knockdown of the inner mitochon

292 ix-targeted photoactivatable GFP showed that mitochondrial fusion was not inhibited in patient fibrob

293 When mitochondrial fusion was prevented in starved cells, FAs

294 expression, which plays an essential role in mitochondrial fusion, was observed in TDP-43PrP mice.

295 e mitofusins Mfn1 and Mfn2 are essential for mitochondrial fusion, we deleted these genes from a subs

296 ial step toward determining the mechanism of mitochondrial fusion, we have captured this event in vit

297 To examine the role of Mgm1p in mitochondrial fusion, we looked for molecular interactio

298 e that mitofusins and OPA1 are essential for mitochondrial fusion, whereas Fis1 and Drp1 are essentia

299 eneration via enhancing mitofusin-associated mitochondrial fusion, which provides new insights into t

300 By contrast, depletion of Opa1 suppressed mitochondrial fusion while sparing transport, and did no