ライフサイエンスコーパス: A-band

1 A band at 3642 cm(-1) in BPR, assigned to the OH stretch

2 A band at 38 kDa reacted with MAb 1.1 whereas a band at

3 A band detected at 1996 cm(-1) in the CO-flushed enzyme

4 A band extracted from a differential display polyacrylam

5 A band gap at the Fermi level, as expected for a Zintl p

6 A band gap of 0.12(2) eV was determined by reflectance s

7 A band in the appropriate molecular weight range was ide

8 A band of 73 kDa was increased in striatal membranes.

9 A band of chondrocytes adjacent to the developing interz

10 A band of free polyP was also visible, suggesting that p

11 A band of heavily labeled, medium-sized CB-immunoreactiv

12 A band of intense rainfall extends more than 1,000 km al

13 A band of reduced reflectivity below the RPE was identif

14 A band of Reelin-positive cells filled the superficial d

15 A band of the same size was also immunopurified from hum

16 A band shift assay was designed to evaluate the influenc

17 A band with the p40 electrophoretic mobility was found t

18 A band-sharing index indicating relatedness was created

19 s show efficient blue (15 A) or green (25-40 A) band-edge photoemission with luminescence quantum yie

20 he bulk region merges to vacuum over a ca. 5 A band with progressive diminution of the density and hy

21 Using CRISPR to ablate A-band variant-specific truncation peptides through intr

22 ne another, and progressed to small, aligned A-band-sized aggregates.

23 of second harmonic generation, which allows A-bands to be imaged independently of T-tubule morpholog

24 e striations were classified into amorphous (A)-bands, associated with accumulations on the rootlet s

25 An A-band TTNtv diminished sarcomere function greater than

26 An A-band TTNtv dose-dependently impaired cardiac microtiss

27 191Lys)] was found to segregate alongside an A-band TTN truncating variant in a pedigree with aggress

28 KLHL40 localizes to the sarcomere I band and A band and binds to nebulin (NEB), a protein frequently

29 sarcomeric locations, I band in the IFM and A band in synchronous muscles.

30 The observed trends for the amide I-III and A bands obtained by single-pass ATR-FT-IR agreed with th

31 required for the assembly of the M-band and A-band and for the regular alignment of the network SR a

32 urin destabilizes proteins of the M-band and A-band but not of the Z-disk.

33 cteristics of sparks found in the Z-line and A-band zones were very similar, whereas sparks from the

34 s truncations in the Z disk (TTN-Z(-/-)) and A-band (TTN-A(-/-)) regions of the TTN gene in human ind

35 M-bands and A-bands, but not Z-disks or I-bands, were disrupted when

36 embly, including the assembly of Z-discs and A-bands, but not for early steps such as the assembly of

37 nd PCAF associate with the Z-disc and I- and A-bands of cardiac sarcomeres.

38 I- and A-bands were clearly observed, and thick filaments were

39 action contributes to the assembly of M- and A-bands.

40 ugar chains, the homopolymer common antigen (A band) and the heteropolymer O antigen (B band), which

41 n associated with structural localization as A-band variants overlapping myosin heavy chain-binding d

42 SN-5 antibody colocalized with paramyosin at A-bands in wild type and colocalized with abnormal accum

43 Genetic deletion of the I-band-A-band junction (IAjxn) in titin increases strain on the

44 tin type 3 domains that comprises the I-band/A-band (IA) junction and obtained a viable mouse model.

45 ends of both proteins overlap at the I-band/A-band border, revealing a staggered organisation of the

46 ducing myofibrils with well defined I bands, A bands, and H zones.

47 e discuss the possible relationships between A-band arrangements in successive sarcomeres along a myo

48 -cleaved muscles contract, myosin-containing A-bands become split and adjacent myosin filaments move

49 the spacing between centroids of contiguous A-bands.

50 The LMNA/Titin deletion A-band mice had no functional differences compared with

51 ere insufficiency in the LMNA/Titin deletion A-band mice.

52 ozygous digenic (LMNA [lamin]/titin deletion A-band) with monogenic (LMNA/wild-type) and wild-type/wi

53 The different A-band organisation in flies compared with Lethocerus, w

54 attice of myosin filaments in the Drosophila A-band.

55 In the relaxed state, the dynamic A-band lattice spacing change as a result of a 2 % step

56 ansients and disrupts myosin thick filament (A band) assembly.

57 tis elegans, the gene unc-89 is required for A-band organization of striated muscle.

58 ously excite second harmonic generation from A-bands of myofibrils and 2-photon fluorescence from flu

59 ics of the Duffy antigen (DARC), glycophorin A, band 3, and GLUT1 were compared under analogous condi

60 t the same nine axial positions in each half A-band, consistent with a circumferential and/or radial

61 116 nm, are axially shifted in the hexagonal A-band lattice by one-third of the 14.5 nm axial spacing

62 arranged systematically within the hexagonal A-band lattice of myosin filaments, can redistribute thr

63 hown to increase myosin rod length, increase A-band and sarcomere length, and decrease flight perform

64 responds to mainly physiologically inelastic A-band part of the protein, and for a proteolytic fragme

65 med, the muscle myosin became organized into A-bands, and the cells began beating.

66 which thick filaments are not organized into A-bands, and there are no M-lines.

67 Structurally, the longer A-band and sarcomere lengths found in the hinge B myofib

68 h of the 1.6 mum filaments present in mature A-bands.

69 wever, EM of muscle fibers showed misaligned A-bands.

70 the actin filaments in the bony fish muscle A-band cell unit.

71 e systematically arranged in the fish muscle A-band lattice relative to the myosin head positions, an

72 of troponin molecules in the resting muscle A-band.

73 each half of the vertebrate striated muscle A-band.

74 dicating that they all arise from the muscle A-band.

75 hin is a giant polypeptide located in muscle A-bands.

76 unc-89 results in disorganization of muscle A-bands.

77 Adjacent myosin filaments in striated muscle A-bands are cross-linked by the M-band.

78 tion requires the presence of B-band but not A-band lipopolysaccharide.

79 A novel A-band titin mutation, c.92167C>T (p.P30723S), was found

80 us for the FINmaj TMD mutation and the novel A-band titin missense mutation showed a phenotype comple

81 ts interspersed within the overlap region of A bands and even within the H zone.

82 -band titin ON, the periodic interactions of A-band titin with myosin motors alter their resting disp

83 ere stretch therefore results in movement of A-band titin with respect to the thick filament backbone

84 The stiffness of A-band titin was found to be high, relative to that of I

85 to obtain the axial density distribution of A-bands in electron micrographs of well-preserved specim

86 d around Z-disk analogues and to the edge of A-bands.

87 ntricular myocytes localized to the level of A-bands in sarcomeres, and Myo18a knockout embryos at da

88 y, this antiserum localizes to the middle of A-bands, consistent with UNC-89 being a structural compo

89 -C and -D isoforms localize to the middle of A-bands, like previously-described UNC-89 antibodies, an

90 of MyBP-C slow that reside in the C-zones of A-bands, variant-1 preferentially concentrates around M-

91 s in the Ca2+ content of the mitochondria or A band.

92 roduction in a pslB mutant and pslB promoted A-band LPS synthesis in a wbpW mutant, indicating functi

93 was determined by integrating the respective A-band intensity peak and computing the location at whic

94 with image processing confirm that the same A-band superlattice occurs in all of these flies; it may

95 e strain-sensing via titin in the sarcomeric A-band as the basis for length-dependent activation, tit

96 alize the protein with MHC to the sarcomeric A-band in immunostained muscles.

97 ion of UNC-89 is to help organize sarcomeric A-bands, especially M-lines.

98 r-resolution microscopy reveals extra, short-A-bands lying close to the outer muscle cell membrane an

99 We show that cardiac and skeletal A-bands are very similar, with a length of 1.58+/-0.01 m

100 le cell membrane and between normally spaced A-bands.

101 functionally belongs to the relatively stiff A-band region of titin.

102 It is noteworthy that A-band LPS is selectively maintained on the P. aeruginos

103 In the variant S65T/H148D, the A band absorbance maximum is red-shifted to approximatel

104 concomitant with crossbridge binding in the A band.

105 calization from the Z band to the tip of the A band in these muscles.

106 7 to 9 transverse lines in a portion of the A band where crossbridges are found (C zone).

107 es, we found that HDAC3 was localized to the A band of sarcomeres and was capable of deacetylating my

108 etailed in the accompanying papers, when the A band is excited, green fluorescence appears with a ris

109 fferent kinetics are measured in each of the A bands for times shorter than the characteristic time o

110 ized by immunofluorescence microscopy to the A bands of body-wall muscles, but not the pharynx.

111 the myosin molecules represented within the A bands.

112 that, in addition to interference across the A-band, which must be occurring, the observed meridional

113 cells, has the same primary sequence as the A-band O antigen of Pseudomonas aeruginosa, except that

114 us work on single rigor cross-bridges at the A-band periphery where the myosin concentration is low s

115 -band architecture and also localizes at the A-band, where it interacts with both actin and myosin to

116 calized at the Z-line, whereas OGA is at the A-band.

117 ults indicate that titin compresses both the A-band and Z-disk lattice spacing with viscoelastic beha

118 By EM, the A-band and both Z-band lattice spacings varied with temp

119 f Pseudomonas aeruginosa PAO1 (expresses the A-band and B-band of O antigen) and AK1401 (expresses th

120 band of O antigen) and AK1401 (expresses the A-band but not the B-band) to silicon were investigated

121 main pairs A164-A165 and A168-A169, from the A-band of the giant muscle protein titin, reveal that th

122 and discuss the transition of titin from the A-band to the Z-band.

123 ned with abnormal localization away from the A-band towards the Z-disk of the sarcomere.

124 filament lattice spacing was measured in the A-band (d(1,0)) and Z-disk (d(Z)) regions of the sarcome

125 equencing, we explain why truncations in the A-band domain of TTN cause DCM, whereas truncations in t

126 on is low suggests molecular crowding in the A-band promotes occupancy of the straight myosin conform

127 oncept of cardiac troponin I function in the A-band region of the sarcomere and potential signaling t

128 n and interaction of actin and myosin in the A-band, I-band, and Z-disc and demonstrates that a-actin

129 load increase to the myosin filament in the A-band.

130 in the hexagonal lattice of filaments in the A-band.

131 ows for the usual elastic positioning of the A-band in the final sarcomere, whereas the transduction

132 nd and may extend into the outer edge of the A-band in the obliquely striated muscle of the nematode.

133 the integrity and central positioning of the A-band in the sarcomere and it may act as a template upo

134 , the review discusses the importance of the A-band region of titin in setting thick filament length

135 ccessory protein stripes in each half of the A-band spaced axially at 43-nm intervals and starting at

136 There must be structural features of the A-band that have not yet been described.

137 CRISPR-mediated reading frame repair of the A-band TTNtv restored functional deficits, and could be

138 CRISPR-mediated reading frame repair of the A-band TTNtv restored functional deficits, and could be

139 bout 1 nm inwards (towards the center of the A-band) at low velocity shortening (around 0.9 T0): thei

140 oth proteins colocalize in the C-zone of the A-band, with MyBP-HL enriched closer to the M-line.

141 the myosin heads, at least at the end of the A-band.

142 Projectin is located at the beginning of the A-band.

143 nine sites, 43nm apart, in each half of the A-band.

144 full-length TTN haploinsufficiency, only the A-band TTNtv produced TTN truncation peptides that impai

145 and skeletal muscles and compare this to the A-band structure in cardiac muscle of MyBP-C-deficient m

146 We observed a small volume within the A-band ( approximately 10(-15) L) by confocal microscopy

147 ological hotspots were identified within the A-band and N-terminal I-band that closely correlated wit

148 Pathological hotspots within the A-band of TTN may be informative in determining variant

149 nvestigate the distribution of MyBP-C in the A-bands of cardiac and skeletal muscles and compare this

150 olecules of the giant protein titin span the A-bands and I-bands that make up striated muscle.

151 binding region fails to localize throughout A-bands.

152 iomyopathy were overrepresented in the titin A-band but were absent from the Z-disk and M-band region

153 um mapped the AB105 antigen predominantly to A bands of myofibrils within Purkinje fibers.

154 alyses, we found that HDAC3 was localized to A-band of sarcomeres and capable of deacetylating myosin

155 ic wavelengths of UVR across the UV-B and UV-A bands found in natural sunlight.

156 Demonstrating why A-band variants are highly pathogenic for DCM could reve

157 nsverse striations that are in register with A-bands.

158 odels harboring DCM-associated TTNtvs within A-band and I-band structural domains using induced pluri