ライフサイエンスコーパス: melanization

1 ggered by appressorium turgor generation and melanization.

2 hila melanogaster serpin 27A, a regulator of melanization.

3 ether determine the pattern and intensity of melanization.

4 nocyte material with increased keratinocytic melanization.

5 ted proteins that have a significant role in melanization.

6 tissues contain substrate for C. neoformans melanization.

7 f a single gene can result in a new level of melanization.

8 and their growth in pigeon excreta supported melanization.

9 te, capsule size, proteinase production, and melanization.

10 repair after irradiation enhances UV-induced melanization.

11 e and/or the repair of this damage increases melanization.

12 trol of immune effectors, hematopoiesis, and melanization.

13 ding; its role is to limit infection-induced melanization.

14 host defense systems: the AMP production and melanization.

15 oes, suggesting a specific role for pathogen melanization.

16 host defense systems: the AMP production and melanization.

17 panied by larger capsules and faster time to melanization.

18 squito Aedes aegypti, there are two distinct melanization activation pathways carried out by differen

19 ography followed by bioassays indicated that melanization activity was primarily associated with a hi

20 nophages within the stroma and basaloid cell melanization also contributed to pigmentation.

21 on of the yellow gene, which is required for melanization, among distantly related Drosophila species

22 Melanization, an insect immune response, requires a set

23 suppresses defects of gpa1 mutation in both melanization and capsule formation, the phenotypes regul

24 extracellular protease cascades, leading to melanization and clotting, and intracellular signal tran

25 Ookinete melanization and hemolymph phenoloxidase activity were f

26 sites exhibited markedly increased epidermal melanization and increased numbers of melanocytes.

27 ntia nigra from the LND cases showed reduced melanization and reduced immunoreactivity for tyrosine h

28 his study revealed the complexity underlying melanization and Toll pathway in mosquitoes.

29 PN6 acts on parasite clearance by inhibiting melanization and/or promoting parasite lysis.

30 butable to polysaccharide capsule formation, melanization, and antibody binding may affect C. neoform

31 ontributions of the capsular polysaccharide, melanization, and antibody binding to the capsule to the

32 mination and appressorium formation, blocked melanization, and caused the formation of abnormal appre

33 d dendrite formation, enhanced melanogenesis/melanization, and cell cycle arrest impact the ability o

34 bial peptide (AMP) production, phagocytosis, melanization, and encapsulation.

35 attributes-polysaccharide capsule formation, melanization, and growth at body temperature.

36 fects of glyphosate on C. neoformans growth, melanization, and murine infection.

37 In Drosophila, the serpin Spn27A regulates melanization apparently by inhibiting the protease that

38 r in association with the lymph gland, while melanizations are located in the gut, salivary gland, an

39 quence of alpha-MSH stimulation is increased melanization attributable to induction of pigmentation e

40 Melanization before infection did not increase resistanc

41 elanin synthesis, reversed the inhibition of melanization but did not restore appressorium formation.

42 coagulation, phagocytosis, encapsulation and melanization but not the slow-response induction of anti

43 enes are known to be necessary for cuticular melanization, but the involvement of these genes in mela

44 ents suggested this viral protein suppresses melanization by more than one mechanism.

45 Tracheal melanization can be activated by the presence of microor

46 ts provide strong evidence that cryptococcal melanization can influence the immune response to infect

47 lirin is implicated in the regulation of the melanization cascade in P. argus by inhibiting peptidase

48 erine proteases, MP1 and MP2, which act in a melanization cascade regulated by Spn27A.

49 The melanization cascade, activated by the prophenoloxidase

50 lirus argus with regulatory functions on the melanization cascade.

51 s of PGRP-LC controls the IMD activation and melanization cascades in Drosophila.

52 nd fungi may therefore trigger two different melanization cascades that use MP1 as a common downstrea

53 eral genes have been shown to play a role in melanization, changes in a single gene - the one encodin

54 To assess the role of the HPS3 protein in melanization, cultured melanocytes developed from HPS-3

55 d for wing expansion, cuticle hardening, and melanization during development.

56 Flies lacking dawdle function exhibit melanization even when uninfected.

57 Tissue melanization, exemplified by the formation of melanotic

58 linkage map, featuring the network of known melanization genes, serves as a resource for melanism re

59 We conclude that wound melanization i) is an important part of innate immunity

60 Lack of melanization in both lineages was associated with loss-o

61 oformans melanin is negatively charged, (iv) melanization in C. neoformans is associated with an incr

62 Melanization in C. neoformans is dependent on five addit

63 MP1 is required to activate melanization in response to both bacterial and fungal in

64 ionship may facilitate appropriate epidermal melanization in response to UV-induced DNA damage.

65 The loss of wound melanization in T. anophthalmus was an apomorphy associa

66 active portion of LPS in mammals, activated melanization in the silkworm Bombyx morii.

67 The results suggest that inhibition of melanization in vivo may facilitate control of C. neofor

68 implicated in the regulation of laccase and melanization, including IPC1, GPA1, MET3, and STE12.

69 Melanization interfered with phagocytosis in vivo for en

70 Melanization is a potent immune response mediated by phe

71 Yet, melanization is an important component of wound healing

72 To learn whether the decline in melanization is associated with a shift from constitutiv

73 Melanization is associated with virulence, but there is

74 times during arthropod evolution, indicating melanization is not an indispensable component of wound

75 erial challenge as controls, indicating that melanization is not essential for defense against bacter

76 an essential factor for Plasmodium ookinete melanization, is also required for melanization of bacte

77 tion of the phenoloxidase cascade leading to melanization, nodule formation, and upregulation of anti

78 However, CLIPA8 is not required for wound melanization nor for melanotic pseudotumor formation in

79 ive leucine-rich repeat protein 1] prevented melanization of 7G8 parasites, reverting the refractory

80 ookinete melanization, is also required for melanization of bacteria in adult mosquitoes.

81 ce inhibits pro-phenoloxidase activation and melanization of bacteria in the hemolymph following micr

82 The phenoloxidase (PO) cascade regulates the melanization of blood (hemolymph) in insects and other a

83 ork nor the cellular interactions underlying melanization of C. neoformans have yielded to comprehens

84 Melanization of C. neoformans in the presence of L-dopa

85 mber, Egf1.0, was recently shown to suppress melanization of hemolymph in Manduca sexta in part by in

86 ike protein 8 (TSVP-8) indicated it inhibits melanization of host hemolymph in vitro, while two predi

87 ) histochemistry demonstrated an increase in melanization of melanosomes.

88 vels of reactive oxygen species, which favor melanization of parasites as well as Sephadex beads.

89 ions of TH and DDC are involved in the pupal melanization of S. exigua.

90 Glycerol accumulation and melanization of the appressorium cell wall collectively

91 genes affecting catecholamine biosynthesis, melanization of the cuticle, and many additional pleiotr

92 requirement of obligatory catecholamines for melanization of the pathogenic fungus Cryptococcus neofo

93 to mice infected with C. neoformans delayed melanization of yeast cells in vivo and prolonged averag

94 free radical formation, taken as an index of melanization, of C. neoformans 24067 cells growing in me

95 promote destruction of pathogens by means of melanization or expression of antimicrobial peptides.

96 However, the mechanisms underlying melanization pathways are not completely characterized.

97 w in the pupae exactly foreshadows the adult melanization pattern in the abdomen of both species, sug

98 ith histological alterations and an abnormal melanization pattern of the limb, indicate altered dorsa

99 results show that the establishment of wing melanization patterns in Drosophila depends on the veins

100 ed serine protease inhibitor, suppresses the melanization phenotype induced by mutant CHMP2B in the f

101 Capsular and melanization phenotypes are associated with virulence.

102 zation reactions that characterize microbial melanization processes.

103 of melanotic tumors, is controlled by tissue melanization protease (CLIPB8), IMP-1, and Serpin-2.

104 ce in mice, capsule size, colony morphology, melanization, protease production, MICs of antifungal dr

105 Immune melanization proteases (IMP-1 and IMP-2) and Serpin-1 me

106 not survive when incubated with amoebae, but melanization protected these cells against killing by am

107 We have also shown that the melanization reaction activated by MP1 and MP2 plays an

108 Here, we describe that the melanization reaction implicated in host defense is acti

109 The melanization reaction is used as an immune mechanism in

110 The melanization reaction of insects requires activation of

111 whereas incubation of WSSV with an in vitro melanization reaction prior to injection into shrimp sig

112 The melanization reaction promoted by the prophenoloxidase-a

113 rge noncovalent complex, which localizes the melanization reaction to the surface of invading microor

114 phenoloxidases (PPOs) are key enzymes of the melanization reaction, which is a prominent defense mech

115 functions downstream of TEP1 to regulate the melanization reaction.

116 The ontogeny of this ectopic melanization resembled that found in Drosophila species

117 CLIPA14 kd mosquitoes elicited a potent melanization response against Plasmodium berghei ookinet

118 de and indicate that suppression of the host melanization response is functionally important for both

119 Pathogens often suppress the melanization response of host insects, but the underlyin

120 ome pathogens are capable of suppressing the melanization response of host insects, but the virulence

121 timicrobial peptide genes and suppresses the melanization response to the nematode.

122 n of infection foci-together with the host's melanization response, formed the basis of H. zea's resi

123 nhibitor that strongly suppresses the insect melanization response.

124 factors responsible for disabling the insect melanization response.

125 these two SPHs act in concert to control the melanization response.

126 CLIP as key activators or suppressors of the melanization responses of Anopheles gambiae to Plasmodiu

127 our current understanding of the An. gambiae melanization responses to Plasmodium.

128 Unexpectedly, we found that tracheal melanization resulting from Spn77Ba disruption induces s

129 lly-significant differences as a function of melanization status occurred in CN.

130 elanomas undergo a characteristic decline in melanization that may reflect altered contributions of k

131 the hemocyte-mediated encapsulation and into melanizations that are not encapsulated by hemocytes.

132 otes yellow pigment formation and suppresses melanization, the expression difference and genetic asso

133 nous obligatory catecholamine precursors for melanization to produce isotopically enriched pigment "g

134 zed in the hemocoel, but the contribution of melanization to survival after bacterial infections has

135 Melanization was slower at 37 degrees C. but by day 14,

136 The speed of wound melanization was uncorrelated with a difference in metab

137 In arthropods, they regulate melanization, which plays an important role in immune de

138 As in extant birds, the extensive melanization would have provided structural advantages t