ライフサイエンスコーパス: depolymerase

1 3 motor protein MCAK is a potent microtubule depolymerase.

2 aZ2 is thus suggested to be an intracellular depolymerase.

3 2a is a member of the Kinesin-13 microtubule depolymerases.

4 ics and mitotic progression by regulating MT depolymerases.

5 ted motors that are proposed to be either MT depolymerases [3, 4, 8, 10, 11] or MT capping proteins [

6 s end-directed motor and a plus end-specific depolymerase--a unique combination of activities not fou

7 Extracellular depolymerase activities and expression of the correspond

8 chromosome movement and that the microtubule depolymerase activities of Kif2a, Kif2b, and MCAK fulfil

9 associated kinesin (MCAK) and inhibits their depolymerase activities.

10 regulatory mechanism underlying precise MCAK depolymerase activity control during mitosis remains elu

11 CAK at Ser715 which promotes its microtubule depolymerase activity essential for faithful chromosome

12 This unanticipated amyloid-depolymerase activity is conserved from yeast to humans,

13 Here we demonstrate that the depolymerase activity is indispensable to control spindl

14 with a kinesin-5-mediated, length-dependent depolymerase activity that organizes chromosomes at the

15 sary and sufficient for plus-end binding and depolymerase activity, as well as by the identification

16 pD, a gamma-glutamyltranspeptidase with PDGA depolymerase activity.

17 ture is required for the elaboration of PDGA depolymerase activity.

18 somal passenger complex (CPC) regulate Kif2a depolymerase activity.

19 AK on residues that regulate its microtubule depolymerase activity.

20 ability during mitosis by inhibiting MCAK MT depolymerase activity.

21 The chitin depolymerases also had a specific pattern of activity to

22 ment end, which, when occupied, has both the depolymerase and ATPase activities.

23 l xylan esterases, poly (3-hydroxyalkanoate) depolymerases and CEs, and proteins of unknown function

24 aZ1(b), and PhaZ1(c) (putative intracellular depolymerases), as well as PhaZ2 (a hydroxybutyrate olig

25 duction of cell wall-degrading enzymes (wall depolymerases) by plant pathogenic fungi is under catabo

26 olytic system includes three secreted chitin depolymerases (ChiA, ChiB, and ChiC), a secreted chitin-

27 c and proteomic analyses reveal 13 cellulose depolymerases complemented by seven accessory enzymes, i

28 cellular poly[D-(-)-3-hydroxybutyrate] (PHB) depolymerases degrade PHB granules to oligomers and mono

29 dation analysis using cellubiuronan-specific depolymerase demonstrated that the oligosaccharide-lipid

30 genes predicted to encode intracellular PHB depolymerases (depA and depB).

31 bacter species possess a Vi antigen-specific depolymerase enzyme missing in S enterica Typhi, and we

32 sults demonstrate this phage and its capsule depolymerase exhibit specificity for capsular type K1 an

33 ersity and specificity within the kinesin-13 depolymerase family.

34 olecular weight product by a type 3-specific depolymerase from Bacillus circulans.

35 l of using the poly(3-hydroxybutyrate), PHB, depolymerase from Psuedomonas lemoignei in organic media

36 Recently an intracellular PHB depolymerase gene (phaZ1) from Ralstonia eutropha was id

37 e now report identification of candidate PHB depolymerase genes from R. eutropha, namely, phaZ2 and p

38 nome were used to identify two new candidate depolymerase genes in R. eutropha: phaZ2 and phaZ3.

39 phaZ1 was used to identify two candidate depolymerase genes in the genome of Ralstonia metallidur

40 e currently known polyhydroxyalkanoate (PHA) depolymerases have lipase activity, they do have a catal

41 The KinI kinesin MCAK is a microtubule depolymerase important for governing spindle microtubule

42 e general function of kinesin-13 microtubule depolymerases in preventing ectopic, spontaneous microtu

43 ization is controlled in part by microtubule depolymerases, including the kinesin-13 family of protei

44 The KinI kinesin MCAK, a microtubule depolymerase, is critical for this regulation.

45 Here the authors show that the microtubule depolymerase Kif2 is localized to a cortical subdomain o

46 This study shows that the microtubule depolymerase Kif2 is localized to a cortical subdomain o

47 Here we show that the microtubule depolymerase Kif2 localizes to this subdomain of cortica

48 Mechanistically, DDA3 interacts with the MT depolymerase Kif2a in an MT-dependent manner and recruit

49 regions of the kinesin-13 family microtubule depolymerases Kif2a and mitotic centromere-associated ki

50 localization and binding to the microtubule depolymerase Kif2b, and for NuMA binding to dynein.

51 rates for kinesin translocase motors and for depolymerase kinesins.

52 kinesin (Cin8, class Kin-5), together with a depolymerase (Kip3, class Kin-8) or minus-end-directed k

53 s dynamically unstable ipMTs outward, the MT depolymerase KLP10A acts at the poles to convert ipMT sl

54 n patronin, which antagonizes the kinesin-13 depolymerase KLP10A at spindle poles, thereby switching

55 depletion of the pole-associated microtubule depolymerase KLP10A increased spindle microtubule densit

56 irectly by localizing the pole-associated MT depolymerase KLP10A.

57 gh the actions of the Kinesin-13 microtubule depolymerase, leading to a sparse interphase microtubule

58 or a polar "pulling-in" mechanism in which a depolymerase localized at kinetochore fiber minus ends m

59 Kip3p (kinesin-8), a MT depolymerase, may be implicated, but other molecular det

60 The MT depolymerase MCAK (mitotic centromere-associated kinesin

61 lished a direct link between the microtubule depolymerase MCAK and Aurora B kinase.

62 mulator (ICIS), which stimulates the related depolymerase MCAK, can reactivate Kif2a after Aurora B i

63 on and catalytic activity of the microtubule depolymerase MCAK.

64 Despite extensive study, the kinesin-8 depolymerase mechanism remains under debate.

65 oes cause mislocalization of the microtubule depolymerase mitotic centromere- associated kinesin and

66 The microtubule depolymerase mitotic centromere-associated kinesin (MCAK

67 rora B kinase and the kinesin-13 microtubule depolymerase mitotic-centromere-associated kinesin (MCAK

68 show that Klp10A also acts as a microtubule depolymerase on centriolar microtubules to regulate cent

69 s caused accumulation of MCAK, a microtubule depolymerase, on the spindle, indicating misregulation o

70 odulate plus-end MT dynamics by acting as MT depolymerases or as MT plus-end capping proteins.

71 cemic lactides has been studied with the PHB-depolymerase (P. lemoignei) in organic solvents.

72 The selectivity of the PHB-depolymerase (P. lemoignei) to catalyze the propylation

73 ltifunctional motor protein with microtubule depolymerase, plus-end motility, and antiparallel slidin

74 ncy by the kinetochore-associated kinesin-13 depolymerase promotes metaphase chromosome oscillations;

75 onstrate that Kif2a may act as a microtubule depolymerase, regulating microtubule dynamics, spindle a

76 lts, we propose that ExsH is a succinoglycan depolymerase secreted by a Type I secretion system compo

77 date a heretofore-unrecognized human amyloid-depolymerase system that could have applications in vari

78 ure of one CE1 gene of A. muscaria matched a depolymerase that degrades the carbon storage molecule p

79 reminiscent of MCAK, which is a microtubule depolymerase that is believed to be a key component of t

80 their bacterial host and many phages produce depolymerases that hydrolyze biofilm extracellular polym

81 Moreover, the ability of the PHB-depolymerase to catalyze the solventless polymerization

82 ux, and the chromokinesin KLP3A inhibits the depolymerase to suppress flux, thereby coupling ipMT sli

83 cetonitrile-d(3)) on the activity of the PHB-depolymerase toward propylation of L-lactide was studied

84 tion of one target, a kinesin-13 microtubule depolymerase, underlies a major phenotype associated wit

85 Each chitin depolymerase was detected in culture supernatants of chi

86 The gene-encoding capsule depolymerase was identified.

87 The depolymerases were modular in nature and contained glyco

88 taphase and metaphase are set by microtubule depolymerases, whereas oscillation and breathing periods

89 2a is a member of the kinesin-13 microtubule depolymerases, which tightly regulate microtubule dynami

90 The kinesin-13 MCAK is a potent MT depolymerase with a complex subcellular localization, ye