ライフサイエンスコーパス: LAMP1

1 LAMP1 and LAMP2 proteins are highly abundant, ubiquitous

2 LAMP1 contains an IgA1-like hinge region with potential

3 d in lysosome associated membrane protein 1 (LAMP1) and is needed for growth of Salmonella induced fi

4 aves lysosome-associated membrane protein 1 (LAMP1) at pHs characteristic of the plasma membrane, ear

5 S-1, lysosome associated membrane protein 1 (LAMP1), and LAMP3 were localized to abnormal large granu

6 ined lysosome-associated membrane protein 1 (LAMP1), suggesting the possibility of OMV convergence wi

7 with lysosome-associated membrane protein 1 (LAMP1)-positive and LysoTracker-positive late phagosomes

8 ar, lysosomal-associated membrane protein 1 (LAMP1)-positive organelles.

9 of lysosomal-associated membrane protein 1 (LAMP1).

10 and lysosome-associated membrane protein 1 (LAMP1).

11 ruit lysosome-associated membrane protein 1 (LAMP1); the mechanism of LAMP1 recruitment remains uncle

12 a normal granular expression; and in HPS-3, LAMP1, and LAMP3 exhibited a distinct less granular and

13 hat undergo internalization and routing to a LAMP1-enriched, lysosome-related organelle.

14 ufficient to pilot the effector to acidified LAMP1-positive lysosomal compartments, where WipB intera

15 mounts of Syntaxin6 and is unable to acquire LAMP1.

16 lla-containing phagosomes (SCP) and acquires LAMP1 by fusing with LAMP1-containing Golgi-derived vesi

17 el mechanism showing how Salmonella acquires LAMP1 through a SipC-Syntaxin6-mediated interaction prob

18 n iga mutant of N. gonorrhoeae cannot affect LAMP1 turnover and its growth in epithelial cells is dra

19 RAB43 expression to the Golgi apparatus and LAMP1(-) cytoplasmic vesicles.

20 formation of LC3-positive autophagosomes and LAMP1-positive lysosomes.

21 ve late endosomes/multivesicular bodies, and LAMP1-positive lysosomes and (b) inhibition of its down-

22 ated membrane glycoproteins (LAMPs) CD63 and LAMP1 and the acid hydrolase cathepsin D.

23 interaction between AP-1 sorting complex and LAMP1 on the surface of the transport vesicles is import

24 1 (Tyrp1), dopachrome tautomerase (Dct), and LAMP1 and 3 localization in HPS-3 melanocytes, as evalua

25 ker nor the endosomal markers EEA1, Hrs, and LAMP1.

26 An elevation of LC3-II and LAMP1 and downregulation of Mfn2 in mitochondrial fracti

27 agy-lysosomal proteins, including LC3-II and LAMP1.

28 t show increased presence of CD63(LAMP3) and LAMP1 indicating enhancement of the endolysosomal compar

29 agy effectors (such as ATG5, ATG12, LC3B and LAMP1) and AMPK-dependent activation of the transcriptio

30 CvpD, and CvpE, labeled the PV membrane and LAMP1-positive vesicles when ectopically expressed as fl

31 ins including the class II MHC molecules and LAMP1, a lysosomal resident protein, as well as CD63 and

32 d pronounced colocalization between MUC4 and LAMP1/LC3 (microtubule-associated protein 1A/1B-light ch

33 discovery of the lysosomal proteins NPC1 and LAMP1 as intracellular receptors for Ebola virus and Las

34 te in all cases intact AP3 being present and LAMP1 trafficking being rescued.

35 n of Lamp1, a lysosmal membrane protein, and LAMP1-positive aggregates; and (5) reduced clearance of

36 acquired the endo-lysosomal markers Rab7 and LAMP1 and underwent exclusive retrograde movement.

37 ein LAMP1 and that the frequency of YopD and LAMP1 association correlated with the level of caspase-1

38 auses inhibition of NK-cell cytotoxicity, as LAMP1 RNA interference (RNAi) cells fail to deliver gran

39 tro by DPPA3(1-60) and to a lesser extent by LAMP1/2.

40 e morphology or degranulation, but it causes LAMP1(+) lysosomes to engorge.

41 ly enhanced T-cell activation [CD69, CD107A (LAMP1), HLA-DR and PD-1(PDCD1) expression] and stimulate

42 nscription, and the expression of CD107a(+) (LAMP1) and granzyme B (GZMB) on CD8(+) T cells.

43 A four-gene classifier combining CEACAM4, LAMP1, PLA2G7, and PLAC8 RNA biomarkers was identified.

44 IgA proteases B1 and B2 cleave LAMP1 and mediate intracellular survival in respiratory

45 IgA proteases B1 and B2 cleave LAMP1.

46 ted that the Neisseria IgA1 protease cleaves LAMP1 (lysosome-associated membrane protein 1), a major

47 was observed for the amplification of CUL4A, LAMP1, TFDP1, and GAS6 genes (P < 0.001).

48 conclusion, our findings suggest that CUL4A, LAMP1, TFDP1, and GAS6 are targets for overexpression an

49 but not laforin (Epm2a(-/-) cells) decreased LAMP1, a lysosomal marker.

50 Rab9 can measurably reverse SifA-dependent LAMP1 recruitment and the perinuclear location of the SC

51 of mice vaccinated with the chimeric Sig/E7/LAMP1 vaccinia remained tumor free 3 months after tumor

52 in early (Rab7 positive) and late endosomal (LAMP1 positive) sorting compartments, before targeting t

53 endo-lysosomal vesicle that is positive for LAMP1.

54 cumulations in neurons [beta-hexosaminidase, LAMP1(lysosome-associated membrane protein 1), SCMAS (su

55 We show here that human LAMP1 and LAMP2 bind cholesterol in a manner that buries

56 xport of APP from the Golgi, and we identify LAMP1(+) structures as the proximal destination of APP a

57 In LAMP1 RNAi cells, more perforin is retained outside of l

58 e of IL-36, IL-36R increased accumulation in LAMP1+ lysosomes.

59 n of myelin-associated glycoprotein (MAG) in LAMP1(+)perinuclear vesicles that fail to migrate to the

60 A single glycosylated residue in LAMP1, present in susceptible species but absent in bird

61 overexpressing AGAP1 also exhibit increased LAMP1 trafficking via the plasma membrane.

62 shRNA in macrophages significantly inhibits LAMP1 recruitment on SCP.

63 ling endosomes, inhibited beta1AR entry into LAMP1(+) lysosomes, and as a result enhanced beta1AR rec

64 A candidate gene from human chromosome 13 is LAMP1, which encodes lysosomal membrane protein 1.

65 imary OLs deficient in Fig4 accumulate large LAMP1(+) and Rab7(+) vesicular structures and exhibit re

66 ion of early p40phox(+) phagosomes into late LAMP1(+) phagosomes.

67 ly (EEA1 and transferrin receptor) and late (LAMP1) endosomes.

68 ive for late endosomal (Rab7) and lysosomal (LAMP1) markers.

69 Autophagic (LC3, p62), lysosomal (LAMP1, cathepsins), and cell death (TUNEL, caspase-3) ma

70 dly elevated markers specific for lysosomes (LAMP1 and LAMP2) and autophagosomes (LC3-II/I).

71 localize with the lysosomal/endosomal marker LAMP1, forming discrete, punctate intracellular vesicles

72 ls, but rather with the late endosome marker LAMP1, as well as with Rab34 GTPase that is known to reg

73 lycogen, the late endosomal/lysosomal marker LAMP1 and the autophagy protein GABARAPL1.

74 uld be colocalized with the lysosomal marker LAMP1 but not with Golgi or nuclear markers.

75 with the appearance of the lysosomal marker LAMP1 on the cell surface, further suggesting the role f

76 ophagy protein LC3, and the lysosomal marker LAMP1 to Mtb-associated structures and are more permissi

77 -SMase colocalized with the lysosomal marker LAMP1, whereas V5-aSMase localized to the Golgi secretor

78 co-localization with the phagolysomal marker LAMP1; this signified altered intracellular trafficking

79 proteins, P62/LC3, and the lysosomal marker, LAMP1.

80 ion of the late phagosome maturation markers LAMP1 and lysosomal cathepsin, indicating delayed format

81 f lysosomes as a result of protease-mediated LAMP1 degradation.

82 presence of CD63 on internal lamellae and of LAMP1 on the membrane surrounding the inclusions, indica

83 Thus, IgA1 protease cleavage of LAMP1 promotes intracellular survival of pathogenic Neis

84 result of IgA1 protease-mediated cleavage of LAMP1.

85 In addition, we observed global collapse of LAMP1(+) lysosomes, with some lysosomal membrane domains

86 ae (GC) increases the rate of degradation of LAMP1, a major integral membrane glycoprotein of late en

87 Disruption of expression of LAMP1 binding partner, adaptor protein 1 (AP-1) sorting

88 eased level of perforin in lytic granules of LAMP1-deficient cells, combined with disturbed motility

89 membrane protein 1 (LAMP1); the mechanism of LAMP1 recruitment remains unclear.

90 Reduction of LAMP1 expression affects the movement of lytic granules

91 sults in IgA1 protease-mediated reduction of LAMP1.

92 AP-3 deficiencies affected the targeting of LAMP1, phosphatidylinositol-4-kinase type II alpha, and

93 n of DAT and leads to accumulation of DAT on LAMP1-positive endosomes.

94 KIP and Rab9 function to maintain peripheral LAMP1 distribution in cells.

95 DCmat infected with rVV-Sig-pp65-LAMP1 induced proliferation of pp65-specific CD4(+) clon

96 reover, infection of DCmat with rVV-Sig-pp65-LAMP1 resulted in at least equivalent presentation to CD

97 brane protein 1 targeting sequence (Sig-pp65-LAMP1) to target pp65 to the class II compartment.

98 ed with the late endosomal/lysosomal protein LAMP1 and that the frequency of YopD and LAMP1 associati

99 uired the late endosome and lysosome protein LAMP1.

100 he major lysosomal integral membrane protein LAMP1 and that this is due to hydrolysis of this glycopr

101 ular receptor, the lysosome-resident protein LAMP1.

102 n the amounts of the late endosomal proteins LAMP1 and CD63 and an increase in the amount of LAMP2.

103 Knockdown of the lysosomal membrane proteins LAMP1 and LAMP2 resulted in decreased cell viability, as

104 , the lysosome-associated membrane proteins, LAMP1 and LAMP2, from Pompe iPSC-CMs demonstrated higher

105 serial type 2 IgA1 protease cleaves purified LAMP1 in vitro.

106 intracellular storage of antigen in Rab11(+)LAMP1(+) compartments.

107 on of late endosomal proteins, such as Rab7, LAMP1, and CD63.

108 ith interactions with the endosomal receptor LAMP1 or interfere at another stage in entry that is com

109 ipB(-), sipD(-), sopB(-), or sopE(-) recruit LAMP1, demonstrating the specificity of SipC in this pro

110 by other intracellular pathogens to recruit LAMP1.

111 nd membrane contents, in addition to reduced LAMP1 membrane recruitment.

112 Therefore, we sequenced LAMP1 cDNAs from homozygous mnd mice and unrelated wildt

113 ned, and expression analysis shows a similar LAMP1 protein distribution in wildtype and mutant mice,

114 ha, BLOC-1, or AP-3 complexes led to similar LAMP1 phenotypes.

115 We found that LAMP1 in the mouse lies within the region of the mnd mut

116 We show that LAMP1 silencing causes inhibition of NK-cell cytotoxicit

117 A1 protease is directly responsible for this LAMP1 degradation.

118 EGF exhibited delayed trafficking of EGF to LAMP1-positive late endosomes and lysosomes and slowed E

119 the cell surface, while IFITM3 localizes to LAMP1-containing compartments.

120 r intracellular compartments but migrates to LAMP1(+) endosomes on stimulation with a TLR3 ligand.

121 ic pH optimum (~4.6) and colocalization with LAMP1 verified lysosomal functioning of ARSK.

122 PRCP antigen does not colocalize with LAMP1 on nonpermeabilized HUVECs, but it partially coloc

123 lls and found the majority colocalizing with LAMP1-positive compartment and not with the peroxisomal

124 omes (SCP) and acquires LAMP1 by fusing with LAMP1-containing Golgi-derived vesicles.

125 e interaction of the virus glycoprotein with LAMP1.

126 ) and early endosome antigen 1, but not with LAMP1 protein.

127 r Tim-3 colocalized with p85 and IRF7 within LAMP1(+) lysosomes, suggestive of a role in degradation.