ライフサイエンスコーパス: cristae

1 n their associated sensory structures (i.e., cristae).

2 development of sensory patches (maculae and cristae).

3 nect the inner boundary membrane to lamellar cristae.

4 x of subunit 4 lack both dimers and lamellar cristae.

5 e on an enlarged appearance with reorganized cristae.

6 ion of highly curved ridges in mitochondrial cristae.

7 membrane and the inner membrane with folded cristae.

8 mal mitochondrial matrix and packed lamellar cristae.

9 membrane proteins that control the shapes of cristae.

10 l-x(L) also localized to inner mitochondrial cristae.

11 ria are swollen and many have no discernible cristae.

12 plete absence of the semicircular canals and cristae.

13 itochondria and remodeling the mitochondrial cristae.

14 semicircular canals, anterior and posterior cristae.

15 circular canals and their associated sensory cristae.

16 ral (CZ) and peripheral (PZ) zones of monkey cristae.

17 he mitochondrial inner matrix, and disrupted cristae.

18 of the mitochondrial matrix and swelling of cristae.

19 chondrial morphology with a loss of internal cristae.

20 and invaginations toward the matrix, called cristae.

21 mitochondria but lacked double membranes or cristae.

22 ish and mice usually involve both canals and cristae.

23 y fated to give rise to sensory cells of the cristae.

24 rcular canals and their sensory tissues, the cristae.

25 of cytochrome c stored in intramitochondrial cristae.

26 e cytochrome c stores (approximately 85%) in cristae.

27 ones of each of the three semicircular canal cristae.

28 a more normal structure with more developed cristae.

29 nd shape changes, focal swelling and loss of cristae.

30 cultured, and possess mitochondria with flat cristae.

31 within the mitochondria, as well as in their cristae.

32 cated on the folded inner membrane, known as cristae.

33 s along the highly curved ridges of lamellar cristae.

34 sponsible for generating the helical tubular cristae.

35 M/TOB) complex and controls the shape of the cristae.

36 ad to the generation of lamellar and tubular cristae.

37 with abnormalities in shapes and numbers of cristae.

38 cated on the folded inner membrane, known as cristae.

39 s have morphologies similar to mitochondrial cristae.

40 ding loss, disorganization and dilatation of cristae.

41 , displayed fragmented mitochondria with few cristae, a less-polarized mitochondrial membrane potenti

42 and Tfam as well as mitochondrial volume and cristae abundance were significantly higher with (-)-epi

43 to the sensory epithelium of the developing cristae ampularis, macula utriculi and macula sacculi of

44 Robust, dark labeling in the cristae ampullares suggested that the vast majority of t

45 Vestibular tissues (cristae ampullares, macular otolithic organs, and Scarpa

46 nit, NR-1 was investigated in the chinchilla cristae ampullaris and utricular maculae at the light an

47 ons of the semicircular canals, known as the cristae ampullaris, but none of the other four sensory o

48 the vasculature throughout the stroma of the cristae ampullaris, the maculae utricle, and saccule in

49 (cellulose versus chitin), and mitochondrial cristae (ancestrally tubular not flat), possibly also pr

50 crystalline inclusions, ii) linearization of cristae and abnormal angular features, iii) concentric l

51 w swelling of mitochondria with disorganized cristae and areas of condensation.

52 ins that maintain the connection between the cristae and boundary membranes.

53 ered structural changes in the mitochondrial cristae and caused increased fragmentation by blocking m

54 Our results show disorganized mitochondrial cristae and degenerating mitochondria in endothelial cel

55 l mitochondria that were devoid of organized cristae and displayed severe membrane abnormalities.

56 etformin triggers the disorganization of the cristae and inner mitochondrial membrane in several canc

57 combination of flat plate-like mitochondrial cristae and kinetocyst-type extrusomes with centrohelids

58 hifts through the parallel remodeling of the cristae and of the MERCs via a mechanism that degrades O

59 SH was associated with loss of mitochondrial cristae and paracrystalline inclusions in 9 of 10 subjec

60 ia, which are fragmented, display remodelled cristae and release cytochrome c, thereby driving apopto

61 o cleave OPA1 resulting in remodeling of the cristae and release of the highly concentrated protons w

62 e absence of Aim24 leads to complete loss of cristae and respiratory complexes.

63 ons passed through cartilages, cartilaginous cristae and ridges on the plantar side of the distal tib

64 embranes failed to form tubular or vesicular cristae and showed as closely packed stacks of membrane

65 e become fused and the junctions between the cristae and the intermembrane space are opened.

66 r diverticula, significant loss in the three cristae and the macula utriculus, and a fused utriculosa

67 mechanoreceptor organs, the utricle/saccule, cristae, and cochlea, with distinct types of acellular m

68 1 vestibular hair cells in ototoxin-damaged cristae, and improved vestibular function.

69 hondrial network fragmentation, disorganised cristae, and increased autophagosomes.

70 th fragmented and tubular cristae or loss of cristae, and reduced crista membrane.

71 a strikingly altered ultrastructure, lack of cristae, and swelling.

72 ed by large invaginations, the mitochondrial cristae, and the inner boundary membrane, which is in pr

73 the circulatory system (auricle, ventricle, cristae aorta, anterior aorta) and the reproductive syst

74 ug on mitochondria viz. disruption of normal cristae architecture and dissipation of mitochondrial tr

75 ates mitochondrial fusion and maintenance of cristae architecture.

76 They also provide evidence that the cristae are a subcompartment of the inner membrane.

77 Instead, cristae are either absent or balloon-shaped, with ATP sy

78 Tubular cristae are formed via invaginations of the inner bounda

79 plexes of oxidative phosphorylation, but how cristae are formed, remained an open question.

80 strongly impaired and irregular, and stacked cristae are present.

81 These IMJs and associated cristae arrays may provide the structural basis to enhan

82 nd Msx1 in prospective lateral and posterior cristae at E11.5.

83 coordination of inner mitochondrial membrane cristae at inter-mitochondrial junctions (IMJs).

84 be generated were the superior and posterior cristae at stage 19, followed by the macula sacculi at s

85 During this process, individual cristae become fused and the junctions between the crist

86 Within individual mitochondria, the cristae become locally rearranged in a pattern that we h

87 Opa1), a mitochondrial GTPase that regulates cristae biogenesis and mitochondria dynamics.

88 (HCs) in squirrel monkey (Saimiri sciureus) cristae by a nearly 3:1 ratio.

89 ial membrane structure (swelling and loss of cristae by electron microscopy).

90 a-reperfusion injury, protects mitochondrial cristae by interacting with cardiolipin on the inner mit

91 nthase dimers and ATP production in inflated cristae by mitofilin down-regulation concomitant to MICO

92 by improving the structure of mitochondrial cristae, can increase the oxidative phosphorylation rate

93 sed of the outer and inner membranes and the cristae cluster, which enclosed the lower density mitoch

94 QIL1 expression rescued cristae defects, and promoted re-accumulation of MICOS s

95 Here, we demonstrate that cristae-deficient mitochondria (mitosomes) of Trachiplei

96 enriched fibres have significantly increased cristae density and that, at the whole-body level, muscl

97 indings establish an elevating mitochondrial cristae density as a regulatory mechanism for increasing

98 engages, the mitochondria network fragments, cristae density drops by 30%, and mitochondrial respirat

99 te dehydrogenase histochemical activity, and cristae density increased.

100 t the whole-body level, muscle mitochondrial cristae density is a better predictor of maximal oxygen

101 trast to the current view, the mitochondrial cristae density is not constant but, instead, exhibits p

102 spirations, ATP synthesis, and mitochondrial cristae density were decreased in cardiac mitochondria a

103 on per mitochondria depends on plasticity in cristae density, although current evidence for such a me

104 ondrial rupture, decreased mitochondrial and cristae density, release of cytochrome C and apoptosis i

105 Formation of lamellar cristae depends on the mitochondrial fusion machinery th

106 ostatic pressure for 3 days induced abnormal cristae depletion and decreased the length of the mitoch

107 ntially reduced cristae volume, and abnormal cristae depletion in 10-month-old glaucomatous ONH axons

108 reduction of COX, mitochondrial fission and cristae depletion, alterations of OPA1 and Dnm1 expressi

109 re triggered mitochondrial fission, abnormal cristae depletion, Drp-1 translocation, and cellular ATP

110 With increasing age, the typical cristae disappear and the inner membrane vesiculates.

111 rated pericytes displaying mitochondria with cristae disruption, 3) degenerated astrocytes and periva

112 xic adaptation is reported as rounding sharp cristae edges and expanding cristae width (ICS) by parti

113 ATP synthase dimers determine sharp cristae edges, whereas trimeric OPA1 tightens ICS outlet

114 risingly, short cilia form in mechanosensory cristae even in the absence of kif3a In contrast to Kif3

115 and FAO, while fission in TE cells leads to cristae expansion, reducing ETC efficiency and promoting

116 s the IMM surface is large, due to extensive cristae folding.

117 se cytochrome c is mostly sequestered within cristae folds but released rapidly and completely during

118 proximately 15 nm, the size of mitochondrial cristae folds.

119 veloped internal membrane structure with few cristae; following 24 h of germination the mitochondria

120 COS assembly, mitochondrial respiration, and cristae formation critical for mitochondrial architectur

121 r structure explains the structural basis of cristae formation in mitochondria, a landmark signature

122 Mic60 is an ancient mechanism, important for cristae formation, and had already evolved before alpha-

123 mitochondrial membrane that is required for cristae formation.

124 tion preserves mitochondrial respiration and cristae formation.

125 animals had abnormal neuronal mitochondrial cristae formation.

126 ructurally damaged mitochondria, with broken cristae in AbetaPP primary neurons.

127 The mitochondrial cristae in CHCM1/CHCHD6-deficient cells become hollow wi

128 In mammalian skeletal muscle, the density of cristae in mitochondria is assumed to be constant.

129 tra-structural defects and loss of organized cristae in mitochondria of the Polg2(-/-) embryos as wel

130 ion and activation of CaMK-II in maculae and cristae in older embryos suggests continued roles in aud

131 oosely packed and disorganized mitochondrial cristae in TGiPLA2gamma mice that were accompanied by de

132 was reduced to 50% suggesting remodeling of cristae in the absence of ChChd3.

133 OPA1 localizes to mitochondrial cristae in the inner membrane where electron transport c

134 itochondria reveal the reorganization of the cristae in three dimensions.

135 d mitochondrial density and size and loss of cristae) in WT, but not kin(-) cells.

136 tivity, increased supercomplexes, and denser cristae, independent of mitochondrial biogenesis.

137 ry (inner boundary membrane) than inside the cristae, indicating high accessibility to cytosol-derive

138 rdiac mitochondria are swollen with abnormal cristae, indicative of metabolic failure, but hallmarks

139 We postulate that FGFs in the cristae induce a canal genesis zone by inducing/upregula

140 3D-reconstruction revealed the highly folded cristae inner membrane, features of functionally active

141 f the highly concentrated protons within the cristae invaginations.

142 The cristae involved in a swirl are deficient in respiratory

143 The structural integrity of mitochondrial cristae is crucial for mitochondrial functions; however,

144 The mitochondrial contact site and cristae junction (CJ) organizing system (MICOS) dynamica

145 lex distribution, and thus, potentially also cristae junction copy number.

146 by narrow, tubular membrane segments called cristae junctions (CJs).

147 MICOS subcomplexes independently localize to cristae junctions and are connected via Mic19, which fun

148 phenomenon of largely horizontally arranged cristae junctions that connect the inner boundary membra

149 se in inner:outer membrane ratio, whereas no cristae junctions were detected.

150 d in the intermembrane space and enriched at cristae junctions.

151 INOS subunit, is preferentially localized at cristae junctions.

152 karyotic membranes, induces the formation of cristae-like plasma membrane invaginations.

153 ut of 80 tested were found to disperse these cristae-like vesicles into single soluble complexes or "

154 ee proteins are localized in highly purified cristae-like vesicles obtained by extensive subfractiona

155 ril degeneration, disorganized mitochondrial cristae, lipid inclusions and vacuolation.

156 vivo functions of Mgm1, membrane fusion and cristae maintenance, and more generally shed light onto

157 s in mitochondrial inner membrane fusion and cristae maintenance.

158 Free NAD(+):NADH ratios in mitochondrial cristae, matrix, and cytosol assessed by metabolite indi

159 xpression patterns, the anterior and lateral cristae may share a common origin.

160 omains of the contiguous inner membrane--the cristae membrane (CM) and the inner boundary membrane (I

161 and required for the establishment of normal cristae membrane architecture.

162 ria that connect the inner boundary with the cristae membrane.

163 TP synthase is more centrally located at the cristae membrane.

164 Pretreatment of rats with SS-31 protected cristae membranes during renal ischemia and prevented mi

165 because ischemia destroys the mitochondrial cristae membranes required for mitochondrial ATP synthes

166 d mitochondria that were virtually devoid of cristae membranes, demonstrating the importance of these

167 ngular features, iii) concentric layering of cristae membranes, iv) matrix compartmentalization, v) n

168 t mitochondrial abnormalities, mostly in the cristae membranes.

169 isplay aberrant mitochondrial inner membrane cristae, mgm1 dnm1 double mutants restore normal inner m

170 cation, suggesting that the sensory tissues, cristae, might induce the formation of their non-sensory

171 associated with MICOS disassembly, abnormal cristae, mild cytochrome c oxidase defect, and sensitivi

172 n of Oma1 restored mitochondrial tubulation, cristae morphogenesis, and apoptotic resistance in cells

173 drial protein named CHCM1 (coiled coil helix cristae morphology 1)/CHCHD6.

174 tion of the TOB/SAM complex leads to altered cristae morphology and a moderate reduction in the numbe

175 is a critical organizer of the mitochondrial cristae morphology and thus indispensable for normal mit

176 P synthase oligomer mutants, exhibit altered cristae morphology even though ATP synthase oligomer for

177 red during hypoxia, and we therefore studied cristae morphology in HepG2 cells adapted to 5% oxygen f

178 ion of wild-type YME1L restored the lamellar cristae morphology of YME1L-deficient mitochondria.

179 MICOS assembly and cristae morphology were not efficiently rescued by over-

180 e MICOS complex, necessary for CJ integrity, cristae morphology, and mitochondrial function and provi

181 HD6 is linked to regulation of mitochondrial cristae morphology, cell growth, ATP production, and oxy

182 liferation and apoptotic resistance, altered cristae morphology, diminished rotenone-sensitive respir

183 Our data suggest that, by altering cristae morphology, fusion in TM cells configures electr

184 ner membrane, crucial for the maintenance of cristae morphology.

185 which is known to also control mitochondrial cristae morphology.

186 kdown causes severe defects in mitochondrial cristae morphology.

187 ma-1 and immt-1 also have similar effects on cristae morphology.

188 iameter are an indirect effect of disrupting cristae morphology.

189 Mfn-knockdown flies also display altered cristae morphology.

190 of unknown function, controls mitochondrial cristae morphology.

191 itochondria and a fundamental determinant of cristae morphology.

192 itochondrial features, including conspicuous cristae, mtDNA, the tricarboxylic acid (TCA) cycle, and

193 A change in the shape of mitochondrial cristae must take place to attain rapid and complete rel

194 vacuolization, swelling, and dissolution of cristae occurred in axons as early as 3 days after sensi

195 At the associated junctions, the cristae of adjacent mitochondria form parallel arrays pe

196 which was absent in reduced or OMM-detached cristae of OPA1- and mitofilin-silenced cells, respectiv

197 completely absent in the apex and all three cristae of the semicircular canal ampullae.

198 eversed between vestibular hair cells in the cristae of the semicircular canals and auditory hair cel

199 The cristae of these fragmented mitochondria are disorganize

200 h factor receptor) is a marker for the three cristae only.

201 mbrane and often appear to be wrapped around cristae or crista-like inner membrane invaginations.

202 al IM structures with fragmented and tubular cristae or loss of cristae, and reduced crista membrane.

203 ial genome but do not preserve mitochondrial cristae or respiratory chain supercomplex assembly in pr

204 species, resistant to genetic disruption of cristae organization, dynamically modulated by mitochond

205 caspase (Smac), alteration of mitochondrial cristae organization, generation of reactive oxygen spec

206 hase, and the mitochondrial contact site and cristae organizing system (MICOS) complex.

207 Mic60) of the mitochondrial contact site and cristae organizing system (MICOS) IMM complex is attache

208 The mitochondrial contact site and cristae organizing system (MICOS) is a recently discover

209 multisubunit mitochondrial contact site and cristae organizing system (MICOS) was found to be a majo

210 ranes and the mitochondrial contact site and cristae organizing system (MICOS).

211 the complex "mitochondrial contact site and cristae organizing system" and its subunits Mic10 to Mic

212 ps2-Mdm35 and mitochondrial contact site and cristae organizing system, in the biosynthesis and trans

213 innervate their hair cell targets within the cristae organs in the double mutants.

214 ity of vestibular sensory innervation to the cristae organs was markedly decreased, compared to wild-

215 ced coexistence of tubular and flat lamellar cristae phases.

216 in affected the structural patterning of the cristae, possibly via a decrease of Msx1 and p75NGFR exp

217 al integrity and biogenesis of mitochondrial cristae remain to be fully elucidated.

218 unds the role and mechanism of mitochondrial cristae remodeling in apoptosis.

219 n mitochondria-ER tethering, thereby linking cristae remodeling to MERC assembly.

220 ochrome c mobilization through Opa1-mediated cristae remodeling.

221 ated protein OPA1 are critical regulators of cristae remodeling.

222 iting apoptosis as genetic interference with cristae remodelling and cytochrome c release.

223 r, OPA1, regulating inner membrane dynamics, cristae remodelling, oxidative phosphorylation, was post

224 t site and inhibit Bid-induced mitochondrial cristae reorganization and cytochrome c release.

225 erization but instead promoted mitochondrial cristae reorganization and membrane lipid peroxidation.

226 ation factors generates concentric ring-like cristae, restores tubular mitochondrial morphology, and

227 Sectioned images of the cristae reveal that they have neither a baffle nor septa

228 rs are found in rows along the highly curved cristae ridges, and appear to be crucial for membrane mo

229 n promote neuronal survival independently of cristae shape, whereas stress-induced OMA1 activation an

230 of respiring mitochondrial networks through cristae stabilization, phosphorylation of chaperones and

231 hearts exhibited a distinctive mitochondrial cristae-stacking abnormality suggestive of a phospholipi

232 initial mitochondrial leak of OPA1 leads to cristae structural alterations and exposure of previousl

233 ip of the inner mitochondrial membrane (IMM) cristae structure and intracristal space (ICS) to oxidat

234 ing a mitochondrial large GTPase involved in cristae structure and mitochondrial network fusion.

235 characterized for its role in mitochondrial cristae structure and organelle fusion, possible effects

236 erations (i.e., enlargement, partial loss of cristae structure) and impairment of respiratory superco

237 ntermembrane space important for maintaining cristae structure, is co-released with cytochrome c.

238 S-OPA1 alone maintained normal mitochondrial cristae structure, which has been commonly assumed to be

239 for maintaining mitochondrial energetics and cristae structure.

240 distended inner membrane and partial loss of cristae structure.

241 c from mitochondria, in part by controlling cristae structures.

242 that Msx-1 is a sensory marker for the three cristae, the lagena, and macula neglecta.

243 lateral otocyst into semicircular canals and cristae through two distinct mechanisms: regulating the

244 activity of OPA1 is critical for maintaining cristae tightness and thus energetic competency.

245 he ATP synthase dimers that form rows at the cristae tips dissociate into monomers in inner-membrane

246 key cellular structures (from mitochondrial cristae to nuclear pores) lie below the diffraction limi

247 The ratio of cristae to outer membrane surface area is large in these

248 Mitochondrial cristae topography and connectivity, matrix volume, and

249 ers of the helical arrays match those of the cristae tubes, suggesting the unique features of the P.

250 Unlike cristae, type II HCs predominate in monkey maculae.

251 it variable respiratory defects and abnormal cristae ultrastructure.

252 stical analysis of cryoelectron tomograms of cristae vesicles isolated from Drosophila flight-muscle

253 sion, matrix swelling, substantially reduced cristae volume, and abnormal cristae depletion in 10-mon

254 gena, saccule, utricle, macula neglecta, and cristae was characterized with an anti-acetylated tubuli

255 came irregular in shape and smaller, and the cristae were decreased and appeared disorganized, with b

256 More than 60 years ago, cristae were discovered as characteristic elements of mi

257 Matrix and cristae were retained but distributed unevenly with less

258 Presynaptic mitochondrial cristae were widened, suggesting a sustained energy dema

259 e sensory organs (the superior and posterior cristae) were found at the limits, or boundaries, of the

260 ies (swelling, pale matrix, and disorganized cristae) were found predominantly in older mutant animal

261 ker for the superior, lateral, and posterior cristae, whereas Fng served as an early marker for the m

262 nanodomains originate from the mitochondrial cristae, which are compressed upon calcium signal propag

263 l expression in central zones of maculae and cristae, which are innervated by phasic neurons that are

264 show both forms to localize to mitochondrial cristae, which contain not only locally curved membranes

265 s rounding sharp cristae edges and expanding cristae width (ICS) by partial mitofilin/Mic60 down-regu

266 hanges in mitochondria (swelling and loss of cristae), with preserved DeltaPsi(m), (2) depolarization

267 development of semicircular canals and lack cristae within the ear, while in van gogh, semicircular