Two pore channel 2 (TPC2) inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH

Yingying Lu; Bai Xia Hao; Richard Graeff; Connie W.M. Wong; Wu Tian Wu; Jianbo Yue

doi:10.1074/jbc.M113.484253

Two pore channel 2 (TPC2) inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH

Yingying Lu, Bai Xia Hao, Richard Graeff, Connie W.M. Wong, Wu Tian Wu, Jianbo Yue

Veterinary and Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

78 Scopus citations

Abstract

Background: The role and mechanism of NAADP, an endogenous Ca2+ mobilizing nucleotide, in autophagic regulation remain to be determined. Results: Activation of NAADP/TPC2 signaling induced the accumulation of autophagosomes. Conclusion: The NAADP/TPC2 signaling inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH. Significance: Development of agonists or antagonists of NAADP should provide a novel approach to specifically manipulate autophagy.

Original language	English (US)
Pages (from-to)	24247-24263
Number of pages	17
Journal	Journal of Biological Chemistry
Volume	288
Issue number	33
DOIs	https://doi.org/10.1074/jbc.M113.484253
State	Published - Aug 16 2013

Access

10.1074/jbc.M113.484253

OpenUrl availability

Full text

Cite this

@article{06052d0a738a495abac694f03c4f66e0,

title = "Two pore channel 2 (TPC2) inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH",

abstract = "Background: The role and mechanism of NAADP, an endogenous Ca2+ mobilizing nucleotide, in autophagic regulation remain to be determined. Results: Activation of NAADP/TPC2 signaling induced the accumulation of autophagosomes. Conclusion: The NAADP/TPC2 signaling inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH. Significance: Development of agonists or antagonists of NAADP should provide a novel approach to specifically manipulate autophagy.",

author = "Yingying Lu and Hao, {Bai Xia} and Richard Graeff and Wong, {Connie W.M.} and Wu, {Wu Tian} and Jianbo Yue",

year = "2013",

month = aug,

day = "16",

doi = "10.1074/jbc.M113.484253",

language = "English (US)",

volume = "288",

pages = "24247--24263",

journal = "Journal of Biological Chemistry",

issn = "0021-9258",

publisher = "American Society for Biochemistry and Molecular Biology Inc.",

number = "33",

}

TY - JOUR

T1 - Two pore channel 2 (TPC2) inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH

AU - Lu, Yingying

AU - Hao, Bai Xia

AU - Graeff, Richard

AU - Wong, Connie W.M.

AU - Wu, Wu Tian

AU - Yue, Jianbo

PY - 2013/8/16

Y1 - 2013/8/16

N2 - Background: The role and mechanism of NAADP, an endogenous Ca2+ mobilizing nucleotide, in autophagic regulation remain to be determined. Results: Activation of NAADP/TPC2 signaling induced the accumulation of autophagosomes. Conclusion: The NAADP/TPC2 signaling inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH. Significance: Development of agonists or antagonists of NAADP should provide a novel approach to specifically manipulate autophagy.

AB - Background: The role and mechanism of NAADP, an endogenous Ca2+ mobilizing nucleotide, in autophagic regulation remain to be determined. Results: Activation of NAADP/TPC2 signaling induced the accumulation of autophagosomes. Conclusion: The NAADP/TPC2 signaling inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH. Significance: Development of agonists or antagonists of NAADP should provide a novel approach to specifically manipulate autophagy.

UR - http://www.scopus.com/inward/record.url?scp=84882362568&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84882362568&partnerID=8YFLogxK

U2 - 10.1074/jbc.M113.484253

DO - 10.1074/jbc.M113.484253

M3 - Article

C2 - 23836916

AN - SCOPUS:84882362568

SN - 0021-9258

VL - 288

SP - 24247

EP - 24263

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 33

ER -

Two pore channel 2 (TPC2) inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH

Abstract

Access

OpenUrl availability

Other files and links

Fingerprint

Cite this