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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 2-thiophenecarbo ximidamide dihydrochloride (ARL 17477) on recombinant human neuronal NOS (nNOS) and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 immunodeficiency syndrome-related lymphoma (ARL).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 We examined a panel of ARLs for A20 alterations.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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