Znt7-null Mice Are More Susceptible to Diet-induced Glucose Intolerance and Insulin Resistance

Beta cell-specific Znt8 deletion in mice causes marked defects in insulin processing, crystallisation and secretion

(2010) N. Wijesekara et al.   DIABETOLOGIA

Over-expression of ZnT7 increases insulin synthesis and secretion in pancreatic β-cells by promoting insulin gene transcription

(2010) Liping Huang et al.   EXPERIMENTAL CELL RESEARCH

Deletion of the mouseSlc30a8gene encoding zinc transporter-8 results in impaired insulin secretion

(2009) Lynley D. Pound et al.   BIOCHEMICAL JOURNAL

Insulin crystallization depends on zinc transporter ZnT8 expression, but is not required for normal glucose homeostasis in mice

(2009) K. Lemaire et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

A Common Nonsynonymous Single Nucleotide Polymorphism in the SLC30A8 Gene Determines ZnT8 Autoantibody Specificity in Type 1 Diabetes

(2008) J. M. Wenzlau et al.   DIABETES

The common SLC30A8 Arg325Trp variant is associated with reduced first-phase insulin release in 846 non-diabetic offspring of type 2 diabetes patients—the EUGENE2 study

(2008) T. W. Boesgaard et al.   DIABETOLOGIA

Expression of the ZNT (SLC30) family members in the epithelium of the mouse prostate during sexual maturation

(2008) Catherine P. Kirschke et al.   JOURNAL OF MOLECULAR HISTOLOGY

Insulin-Like Signaling, Nutrient Homeostasis, and Life Span

(2007) Akiko Taguchi et al.   Annual Review of Physiology