NOD2 is dispensable for ATG16L1 deficiency-mediated resistance to urinary tract infection

Authors

Caihong Wang, Washington University School of Medicine in St. Louis
Xuejun Yuan, Washington University School of Medicine in St. Louis
Emily Ma, Washington University School of Medicine in St. LouisFollow
Graziella R. Mendonsa, Washington University School of Medicine in St. Louis
Theo R. Plantinga, Radboud University
Lambertus A. Kiemeney, Radboud University
Sita H. Vermeulen, Radboud University
Indira U. Mysorekar, Washington University School of Medicine in St. Louis

Journal

Autophagy

Publication Date

2014

Volume

10

Issue

2

Document Type

Open Access Publication

DOI

10.4161/auto.27196

Rights and Permissions

Wang C, Yuan X, Ma E, Mendonsa GR, Plantinga TS, Kiemeney LA, Vermeulen SH, Mysorekar IU. NOD2 is dispensable for ATG16L1 deficiency-mediated resistance to urinary tract infection. Autophagy 2014; 10:331 - 338; http://dx.doi.org/10.4161/auto.27196; PMID: 24384785

Recommended Citation

Wang, Caihong; Yuan, Xuejun; Ma, Emily; Mendonsa, Graziella R.; Plantinga, Theo R.; Kiemeney, Lambertus A.; Vermeulen, Sita H.; and Mysorekar, Indira U., "NOD2 is dispensable for ATG16L1 deficiency-mediated resistance to urinary tract infection." Autophagy. 10, 2. (2014).
https://digitalcommons.wustl.edu/open_access_pubs/2641