ライフサイエンスコーパス: lamin B

1 ilarly but only cyclin A/CDK2 phosphorylates lamin B.

2 bition is only slightly reversed by removing lamin B.

3 an antagonistic relationship between Eg5 and lamin B.

4 yosin X, myosin XIV, kinesin 1, Als2cr4, and lamin B-1.

5 In vitro translated Nup153 and lamin B(3) co-immunoprecipitate, and lamin B(3) interact

6 153 and lamin B(3) co-immunoprecipitate, and lamin B(3) interacts specifically with the C-terminal do

7 replication-competent nuclei, we found that lamin B(3) specifically associates with four polypeptide

8 eport that the intermediate filament protein lamin B, a component of the interphase nuclear lamina, f

9 sible for removal of mitotic phosphates from lamin B, a process required for nuclear lamina reassembl

10 eacetylase 8, but not the structural protein lamin B, also were found in the cytoplasm of the cell.

11 he inner nuclear membrane that binds to both lamin B and chromatin and has a putative role in nuclear

12 nal nuclear membrane protein with N-terminal lamin B and chromatin-binding domains plus a C-terminal

13 competitively inhibited the farnesylation of lamin B and K-RasB peptide substrates, with IC50s of 0.8

14 nfection induced the phosphorylation of both lamin B and PKC.

15 dation of major nuclear polypeptides such as lamin B and poly(ADP-ribose) polymerase.

16 primary mouse erythroblasts expressing only Lamin B and primary human erythroblasts only Lamin A/C.

17 ,749 to inhibit the farnesylation of Ras and lamin B and with a reduction in the susceptibility of en

18 Reduction of lamin-B and other caspase-substrate, such as filamin, in

19 fold greater association with its substrate, lamin B, and a 2.5-fold increase in specific activity af

20 Bcl-2, Bid, poly(ADP-ribose) polymerase, and lamin B, and down-regulated cellular levels of FLICE-lik

21 essential nuclear factors such as lamin A/C, lamin B, and HP1.

22 Antibodies to lamin B are found in individuals with autoimmune disease

23 Lamin B assembled into a matrix-like network in mitosis

24 egative mutant lamin B proteins that disrupt lamin B assembly in interphase nuclei also disrupted spi

25 LBR is a bifunctional protein with both a lamin B binding and a sterol Delta(14)-reductase domain.

26 Although genome-wide lamin-B binding profiles correlate with reduced gene exp

27 -lap was closely correlated with cleavage of lamin B but not with increases in p53/p21 or decreases i

28 ot only disprove several prevailing views of lamin-Bs but also establish a foundation for redefining

29 blood mononuclear cells was measured using a lamin B C-terminus peptide as substrate.

30 suggest two nonexclusive mechanisms by which lamin B can indirectly antagonize Eg5.

31 enopus egg extracts, we found that depleting lamin B caused formation of elongated and multipolar spi

32 activation of caspase-6/Mch2 and subsequent lamin B cleavage.

33 tivation, and poly ADP-ribose polymerase and lamin B cleavage.

34 mAb) resulted in preferential degradation of lamin B compared with lamins A and C.

35 ture from the microtubule spindle and from a lamin B-containing spindle envelope.

36 erin and BAF associated only in histone- and lamin-B-containing fractions.

37 Temporal decreases in bcl-2 and cleavage of lamin B corresponded to the minimal apoptotic response o

38 Lamin B could also function to sequester microtubule pol

39 xpression of Bcl-2 resulted in prevention of lamin B degradation and DNA fragmentation into oligonucl

40 n, and that lamin B phosphorylation preceded lamin B degradation and DNA fragmentation.

41 Significant lamin B degradation was detected as early as 1 h after a

42 Because lamin B does not bind directly to microtubules, it must

43 Because lamin B does not bind to Eg5, our studies suggest two no

44 hat protein kinase C-delta co-localized with lamin B during apoptosis and activation of PKC-delta by

45 vestigate phosphorylation and degradation of lamin B during apoptosis.

46 likely involves the localized recruitment of Lamin B during late anaphase.

47 Chromatin and green fluorescent protein-lamin B dynamics were visualized in a micropipette aspir

48 be extended significantly by a disassembling lamin-B envelope that surrounds the prometaphase spindle

49 iates nuclear rupture with dilution of stiff lamin-B filaments, loss of repair factors, and entry fro

50 proteins and with the C-terminal peptide of lamin B for geranylgeranylation by PGGT-I and for farnes

51 es to the nucleus and phosphorylates nuclear lamin B in response to the PKC activator bryostatin.

52 cluding vimentin, actin, fodrin, moesin, and lamin B in resting peripheral blood T lymphocytes.

53 We found that patterns of lamin B in the filamentous network interacting with both

54 nt human PKC-delta was able to phosphorylate lamin B in vitro suggesting that its actions are direct

55 on of its mitotic nuclear envelope substrate lamin B in vitro.

56 The two factors compete for lamin-B in response to matrix elasticity, knockdown, myo

57 Without lamin B, increased microtubule assembly caused by the re

58 se novel, enhancer-rich domains have limited Lamin B interaction.

59 Lamin B is a component of the membranous spindle matrix

60 We propose that lamin B is a structural component of the long-sought-aft

61 sults indicate that selective degradation of lamin B is an early cellular event in response to activa

62 taII PKC-mediated phosphorylation of nuclear lamin B is important in these events.

63 These data suggest that lamin B is phosphorylated by PKCalpha and proteolyzed be

64 Depleting lamin B led to a very small but statistically significan

65 This raises the possibility that lamin B may be a link to the autoimmune attack that occu

66 he mechanosensitive proteins YAP, Lamin A/C, Lamin B, MRTF-A, and MRTF-B were analyzed on these gradi

67 opic expression of a caspase-3 non-cleavable lamin B mutant blocks nuclear opening formation, histone

68 emerin association with BAF in the chromatin/lamin B "niche." These results reveal direct control of

69 obably cause brain disorganizations found in lamin-B null mice.

70 However, lamin B only very weakly antagonizes Eg5 in mediating po

71 y farnesylated by PFT in the presence of the lamin B peptide competitor.

72 In this study, we use human lamin B phosphorylated at mitosis-specific sites as a su

73 osol from camptothecin-treated cells induced lamin B phosphorylation and degradation in isolated nucl

74 ne specifically inhibits betaII PKC-mediated lamin B phosphorylation and mitotic nuclear lamina disas

75 PKC-delta by caspase 3 was concomitant with lamin B phosphorylation and proteolysis.

76 Elevated lamin B phosphorylation in HSV-1-infected cells was part

77 somerase I inhibitor, camptothecin, and that lamin B phosphorylation preceded lamin B degradation and

78 Lamin B phosphorylation was prevented by the protein kin

79 V5) is capable of nuclear translocation and lamin B phosphorylation.

80 sults thus suggest that axonally synthesized lamin B plays a crucial role in axon maintenance by prom

81 e cleavage of poly(ADP-ribose) polymerase or lamin B, polypeptides that are commonly cleaved in other

82 Inhibition of H-Ras, N-Ras, and lamin B protein processing was observed at concentration

83 Dominant negative mutant lamin B proteins that disrupt lamin B assembly in interp

84 for inducible labeling of ER-MCSs using the Lamin B receptor (LBR) and a generic anchor protein on t

85 tally synchronous with the downregulation of lamin b receptor (LBR) and can be reversed by ectopic ex

86 ed complexes of importin-alpha-16 with human lamin B receptor (LBR) and nurim were examined.

87 Mutations of the lamin B receptor (LBR) have been shown to cause HEM dysp

88 Here we remove three nuclear lamins and the lamin B receptor (LBR) in mouse embryonic stem cells and

89 Lamin B receptor (LBR) is a bifunctional nuclear membran

90 The lamin B receptor (LBR) is a highly unusual inner nuclear

91 Lamin B receptor (LBR) is a polytopic membrane protein r

92 Lamin B receptor (LBR) is a polytopic protein of the nuc

93 The lamin B receptor (LBR) is an integral nuclear envelope p

94 sed that an interaction between Xist RNA and Lamin B receptor (LBR) is necessary and sufficient for X

95 st at the nuclear envelope, where it anchors lamin B receptor (LBR) to the inner membrane, and second

96 h a most probable gene assignment to 1q21.3; lamin B receptor (LBR) was localized to 1q42.1; and lami

97 factors in regulating the gene encoding the lamin B receptor (LBR), an inner nuclear membrane protei

98 Lamin B receptor (LBR), an integral inner nuclear membra

99 o-hybrid screen, the nucleoplasmic domain of lamin B receptor (LBR), an integral protein of the inner

100 ree other known HP1 binding proteins: SP100, lamin B receptor (LBR), and the p150 subunit from chroma

101 that inner nuclear membrane proteins such as lamin B receptor (LBR), MAN1, Lap2beta, and the trans-me

102 tly reduced the levels of LBR mRNA, encoding lamin B receptor (LBR).

103 iated proteins which includes LAP1, LAP2 and lamin B receptor (LBR).

104 nvelope-multivesicular bodies is mediated by lamin B receptor and chromatin decondensation.

105 otein transport from the ER to the INM using Lamin B receptor and Lap2beta as model INM proteins.

106 We found that Lamin B receptor expression was required to attach centr

107 Wang et al question whether Lamin B receptor is required for Xist-mediated silencing

108 Zhao et al. describe how during mitosis, the lamin B receptor migrates to the ER membrane to enhance

109 with the inner nuclear membrane protein LBR (lamin B receptor) and transcriptional coactivators TIF1a

110 LBR (lamin B receptor) is an integral protein of the inner nu

111 Finally, we show that loss of Lamin B receptor, a nuclear envelope protein, leads to d

112 used by mutations in the gene (LBR) encoding lamin B receptor, an evolutionarily conserved inner nucl

113 e show that Xist directly interacts with the Lamin B receptor, an integral component of the nuclear l

114 ry biliary cirrhosis (PBC) recognize LBR, or lamin B receptor, an integral membrane protein of the in

115 ls using the inner nuclear membrane protein, lamin B receptor, fused to green fluorescent protein (LB

116 erentiated HL-60 cells lacking expression of lamin B receptor, which fail to develop lobulated nuclei

117 4-dehydrocholesterol reductase (DHCR14), and lamin-B receptor (LBR), share evolutionary ties with a h

118 sue or matrix stiffness anti-correlates with lamin-B receptor (LBR), which contributes to lipid/stero

119 immunosenecence is caused by age-associated lamin-B reduction specifically in fat body cells, which

120 distribution of the nuclear lamina protein, lamin B, remained unchanged.

121 Depletion of lamin B resulted in defects in spindle assembly.

122 GrnA fails to induce cleavage of caspase-3, lamin B, rho-GTPase, or PARP.

123 ctron microscopy and unique fragmentation of lamin B, suggested this form of cell death to be differe

124 cells with condensed chromatin and disrupted lamin B, suggesting that these cells may be blocked at a

125 U1 small nuclear ribonucleoprotein particle, lamin B, the nuclear mitotic apparatus protein NuMA, DNA

126 Besides lamin B, the spindle matrix contains spindle assembly fa

127 ecruitment of PKC functions to phosphorylate lamin B to help modify the nuclear lamina and promote bu

128 vides a continuous linkage from the nucleus (lamin B) to the cortical cytoskeleton.

129 wall muscle revealed that the mutant A-type lamin, B-type lamins, the Sad1p, UNC-84 domain protein K

130 Furthermore, lamin B was essential for the formation of the mitotic m

131 Phosphorylation of lamin B was inhibited by immunodepletion of PKCalpha fro

132 PKCalpha activity also increased rapidly as lamin B was phosphorylated after initiation of the apopt

133 We found that lamin B was phosphorylated within 1 h after addition of