ライフサイエンスコーパス: ARL

1 ARL (acquired immunodeficiency syndrome (AIDS)-related l

2 ARL 17477 (50 mg/kg i.p.) produced a significant reducti

3 ARL 66096 blocked ADP-induced inhibition of adenylyl cyc

4 ARL proteins share 40-60% sequence identity with the ARF

5 ARL-13 acts synergistically with UNC-119, but antagonist

6 ARL-derived immunoglobulin (Ig) genes are significantly

7 ARL/- CRPC expressed abundant AR mRNA despite diminished

8 All ribotypes, including ARL 002, ARL 027, and ARL 106, were reactive in assays that detec

9 The main findings were: (1) ARL samples contained many strains with a final pH < 4.2

10 osphate ribosylation factor-like protein 13 (ARL-13) encoded by the Caenorhabditis elegans homologue

11 Strains from groups 1 and 2 (ARL, 389 strains; SRS, 358 strains) were previously iden

12 ase functional module, which contains ARL-3, ARL-13, and UNC-119, localizes near the poorly understoo

13 We have evaluated 6 ARL-derived antibodies for binding to human immunodefici

14 both sequences, the last three amino acids, ARL, represent a putative peroxisome targeting signal.

15 ansport, is required to recruit and activate ARL-8 on SVPs.

16 l ribotypes, including ARL 002, ARL 027, and ARL 106, were reactive in assays that detect C. difficil

17 that two conserved small GTPases, ARL-13 and ARL-3, coordinate to regulate IFT and that perturbing th

18 r, 2 of the lymphoma-derived Ig's (ARL-7 and ARL-14) bound strongly to non-HIV-infected cells of vari

19 ylation factor-like protein 13B (ARL13B) and ARL-dependent mislocation of a ciliary-localized bile ac

20 osphate/creative phosphokinase (CP/CPK), and ARL-66096, an antagonist of the ADP P2T(AC) receptor inv

21 tions between human ODA16 homolog HsDAW1 and ARL GTPases are conserved, and these interactions are al

22 rightward displacement of this response, and ARL-67156 did not modify it.

23 beta-methylene adenosine 5'-triphosphate and ARL-67156, an adenosine triphosphatase inhibitor, and we

24 Expression analysis of rice ARFs and ARLs in different tissues, stresses and abscisic acid tr

25 tial for functional overlap between ARFs and ARLs was examined by comparing effects of expression on

26 remarkably specific to Golgi-associated ARF/ARL family GTPases during Shigella infection.

27 provides insights on characteristics of ARF/ARL genes in rice and foxtail millet, which could be dep

28 sequence identity with the ARF proteins, but ARLs can be distinguished from ARFs based on expression

29 nhibition of adenylyl cyclase was blocked by ARL 66096, but not by alpha, beta-MeATP or the P2Y1 rece

30 previous inhibition of ectonucleotidases by ARL-67156 greatly intensified this response (~11-fold th

31 Rescue of arl-13 mutants by ARL-3 depletion is mediated by an HDAC6 deacetylase-depe

32 a concentration-dependent manner, but not by ARL 66096 or alpha, beta-MeATP.

33 rreparable stresses downregulate the ciliary ARLs and release UBC9 to SUMOylate FBF1 at the ciliary b

34 all GTPase functional module, which contains ARL-3, ARL-13, and UNC-119, localizes near the poorly un

35 but it was only slightly affected by CP/CPK, ARL-66096, or A3P5PS.

36 roup corresponds to the previously described ARL-VI.

37 hic profile of patients with newly diagnosed ARL have occurred, with the later time intervals associa

38 antiretroviral therapy in 39 newly diagnosed ARLs and examined protein expression profiles associated

39 2-thiophenecarbo ximidamide dihydrochloride (ARL 17477) on recombinant human neuronal NOS (nNOS) and

40 rated a better outcome with chemotherapy for ARL since the introduction of combination antiretroviral

41 The IC(50) values for ARL 17477 on human recombinant human nNOS and eNOS were

42 Furthermore, ARL-8 directly binds to the UNC-104/KIF1A motor to limit

43 factor, to properly activate another GTPase ARL-3 in cilia, a regulatory process indispensable for c

44 GAP, and microtubule motor-associated GTPase ARL-8, suggesting a close coupling of phagosome fission

45 a novel mechanism that one ciliopathy GTPase ARL-13, as a GEF, coordinates with UNC-119, which may ac

46 nd SUMOylates the C terminus of small GTPase ARL-13, the worm orthologue of ARL13B that mutated in ci

47 The conserved ARF-like small GTPase ARL-8 is localized to SVPs and directly activates UNC-10

48 The conserved ARF-like small GTPase ARL-8 is required specifically for primary siRNA biogene

49 ded continuously to recruit the small GTPase ARL-8 to the phagolysosome for tubulation.

50 Ciliopathy small GTPase ARLs are proposed as prominent ciliary switches, which w

51 we propose that two conserved small GTPases, ARL-13 and ARL-3, coordinate to regulate IFT and that pe

52 On the other hand ARL 66096 (100 nM), a potent P2TAC antagonist and alpha,

53 It is not clear how ARL-8 is activated in this process.

54 upted result in dysfunctional cilia, yet how ARLs are activated remain elusive.

55 his issue of Neuron, Klassen et al. identify ARL-8 GTPase as a regulator of presynaptic assembly.

56 Importantly, ARL-13 acts as a nucleotide exchange factor (GEF) of ARL

57 In ARL, rituximab diminishes the activity of the p38MAPK si

58 To evaluate the role of EBV in ARL pathogenesis, we analyzed viral gene expression and

59 DDX3 protein was highly expressed in ARL/- CRPC, where it bound to AR mRNA.

60 ctively quantified DDX3 and AR expression in ARL/- CRPC.

61 Marrow involvement in ARL correlates with small noncleaved pathology, thromboc

62 In ARLs loss of A20 may be an alternative mechanism of NF-k

63 We further show that excess inactivated ARL-3 compromises ciliogenesis.

64 All ribotypes, including ARL 002, ARL 027, and ARL 106, were reactive in assays t

65 and was reduced by the ecto-ATPase inhibitor ARL-67156 (6-N,N-diethyl-D-beta,gamma-dibromomethyleneAT

66 dophosphate), the ectonucleotidase inhibitor ARL 67156, or the protein phosphatase inhibitor okadaic

67 l as by the selective neuronal NOS inhibitor ARL 17477 (30-600 nmol).

68 ibition of CD39 activity using the inhibitor ARL 67156 partially overcomes T cell hyporesponsiveness

69 r exogenous ATP or an ecto-ATPase inhibitor, ARL-67156, and by exposure of hepatocytes to extracellul

70 n the endothelin-1 model of focal ischaemia, ARL 17477 (1 mg/kg i.v.) significantly attenuated the in

71 ane-associated proteins into cilia and keeps ARL-13 (Arl13b) from leaking out of cilia via the TZ.

72 tions of the traditional average run length (ARL) in reflecting the differences in sampling schemes,

73 carious material from advanced root lesions (ARL), (2) plaque from sound root surfaces of root-caries

74 ncreased GTPgammaS binding to human ARF-like ARL proteins 1, 2, and 3.

75 Herein we report that the ARF-like (ARL) GTPase ARFRP1 functions upstream of two other ARL G

76 sol in cells lacking either of two ARF-like (ARL) GTPases, Arl1p and Arl3p.

77 Although ARF-like (ARL) proteins are very similar in sequence to ARFs, they

78 DP-ribosylation factors (ARFs) and ARF-like (ARL) proteins, distinct functional roles have been infer

79 ding up to six ARF and at least 18 ARF-like (ARL) proteins.

80 ral clades of apicomplexan-related lineages (ARLs) having been described from environmental sequencin

81 ealed the presence of an aromatic-rich loop (ARL) on the presumptive DNA-binding surface of the enzym

82 systemic AIDS-related non-Hodgkin lymphoma (ARL) were treated with concomitant HAART and infusional

83 imately two thirds of AIDS-related lymphoma (ARL) cases are categorized as diffuse large B-cell type,

84 al characteristics of AIDS-related lymphoma (ARL) over the course of the AIDS epidemic.

85 deficiency syndrome (AIDS)-related lymphoma (ARL), we studied 14 cases in which Epstein-Barr virus (E

86 deficiency syndrome (AIDS)-related lymphoma (ARL).

87 immunodeficiency syndrome-related lymphoma (ARL).

88 Although AIDS-related lymphomas (ARLs) are frequently associated with known oncogenic vir

89 AIDS-related lymphomas (ARLs) are high-grade B-cell lymphomas that are frequentl

90 immunodeficiency syndrome-related lymphomas (ARLs) has improved since the era of highly active antire

91 1, delays corpse clearance, and mislocalizes ARL-8 away from lysosomes.

92 In the intraluminal suture model, ARL 17477 at both 1 and 3 mg/kg i.v. failed to reduce th

93 AR-low/negative (ARL/-) CRPC subtypes have recently been characterized an

94 We have identified a new ARL, ARL8, from a fetal cartilage cDNA library.

95 cy syndrome (AIDS)-related lymphoma) and non-ARL cell lines have been examined as in vitro model syst

96 e inhibitor protein (RKIP) expression in non-ARL cells.

97 lued), nuclear transport factor 2, binder of ARL 2, Paxillin, and transcription termination factor I

98 ile UNC-119 can stabilize the GTP binding of ARL-3.

99 at disrupting the regulated GTP-GDP cycle of ARL-8 reduces tubulation by kinesin-1, delays corpse cle

100 Intriguingly, depletion of ARL-3, another ciliary small GTPase, partially suppresse

101 of BORC, promotes the GDP-to-GTP exchange of ARL-8 in vitro and recruits ARL-8 onto SVPs in vivo.

102 se findings revealed a conserved function of ARL GTPases in IFT transport of motile ciliary component

103 Although the cellular functions of ARL proteins remain unclear, the ttn5 phenotype is consi

104 cts as a nucleotide exchange factor (GEF) of ARL-3, while UNC-119 can stabilize the GTP binding of AR

105 made in the understanding and management of ARL but outcomes still remain inferior compared to those

106 l transforming viruses, we profiled a set of ARL samples using whole transcriptome sequencing.

107 ation by controlling the nucleotide state of ARL-8.

108 The expression profiles from a subset of ARL cases were also compared with a matched group of sim

109 ions that totally abolish the SUMOylation of ARL-13 do not affect its established role in ciliogenesi

110 s is responsible for the improved outcome of ARLs in the era of HAART.

111 We examined a panel of ARLs for A20 alterations.

112 id protein that shares homology to the other ARL proteins, especially ARL5.

113 TPase ARFRP1 functions upstream of two other ARL GTPases, ARL1 and ARL5, which in turn recruit golgin

114 e of these are the corallicolids (previously ARL-V), which possess chlorophyll-biosynthesis genes in

115 int host-virus regulatory network of primary ARL tumor samples and expand our understanding of virus-

116 The small G protein ARL-8 inhibits assembly by promoting dissociation, while

117 acterization of an Arf-like small G protein, ARL-8, required during this process.

118 lation factors (ARFs) and ARF-like proteins (ARLs) are part of the ARF family within the RAS superfam

119 ARF-like proteins (ARLs) comprise a functionally distinct group of incomple

120 ARFs in classes I-III and ARF-like proteins (ARLs) in class IV.

121 -GTP exchange of ARL-8 in vitro and recruits ARL-8 onto SVPs in vivo.

122 However, 2 of the lymphoma-derived Ig's (ARL-7 and ARL-14) bound strongly to non-HIV-infected cel

123 ally, DDX3 may be targetable for sensitizing ARL/- CRPC to AR-directed therapies.

124 Conversely, constitutively SUMOylated ARL-13 fully rescues all ciliary defects of arl-13-null

125 These results demonstrate that ARL 17477 protects against global ischaemia in gerbils a

126 We demonstrate that ARL-3 is a unique small GTPase with unusual high intrins

127 en route to its destination, suggesting that ARL-8 acts like a dispersant to prevent premature synapt

128 roles have been inferred from findings that ARLs lack the biochemical or genetic activities characte

129 Compared with HIV-negative cases, the ARL cases had lower bcl-2 and higher CD10 expression, co

130 ed mean percentages of 41.5 and 32.1 for the ARL and SRS samples, respectively.

131 other SF2 enzymes, however, the roles of the ARL in PriA had not been investigated.

132 The position and sequence of the ARL was similar to loops known to couple ATP hydrolysis

133 c interaction map for PriA, showing that the ARL binds replication fork junctions whereas other sites

134 We propose that DNA binding to the ARL allosterically triggers ATP hydrolysis in PriA.

135 Here, we show that changes within the ARL sequence uncouple PriA ATPase activity from DNA bind

136 Thus, ARLs, initially differentiated from ARFs because of thei

137 dibromomethylene-D-adenosine 5-triphosphate (ARL 67156), reduced the [Ca(2+)](i) increase elicited by

138 In this study we have used ARL 66096, a potent antagonist of ADP-induced platelet a

139 replacement of the last 42 amino acids with ARL sequence in F139L decreased markedly the interaction

140 ally with UNC-119, but antagonistically with ARL-3, in regulating ciliogenesis.

141 Records of 369 patients with ARL diagnosed or treated at a single institution from 19

142 essive impact of treatment for patients with ARL receiving chemotherapy with HAART appears transient

143 Studied were 291 patients with ARL, diagnosed and treated at one medical center between

144 Without ARL-8, presynaptic material aggregates en route to its d