Zn(2+) reverses functional deficits in a de novo dopamine transporter variant associated with autism spectrum disorder

Molecular Autism
Peter J HamiltonKevin Erreger

Abstract

Our laboratory recently characterized a novel autism spectrum disorder (ASD)-associated de novo missense mutation in the human dopamine transporter (hDAT) gene SLC6A3 (hDAT T356M). This hDAT variant exhibits dysfunctional forward and reverse transport properties that may contribute to DA dysfunction in ASD. Here, we report that Zn(2+) reverses, at least in part, the functional deficits of ASD-associated hDAT variant T356M. These data suggest that the molecular mechanism targeted by Zn(2+) to restore partial function in hDAT T356M may be a novel therapeutic target to rescue functional deficits in hDAT variants associated with ASD.

References

Jun 1, 1978·Journal of Autism and Childhood Schizophrenia·M J Jackson, P J Garrod
Jan 31, 2002·Proceedings of the National Academy of Sciences of the United States of America·Claus Juul LolandUlrik Gether
Jun 16, 2005·Progress in Neurobiology·David SulzerAurelio Galli
May 11, 2006·Molecular Pharmacology·Kristopher M KahligAurelio Galli
Mar 13, 2009·Biomarkers : Biochemical Indicators of Exposure, Response, and Susceptibility to Chemicals·Scott FaberH M Skip Kingston
Jul 15, 2011·Pharmacological Reviews·Anders S KristensenUlrik Gether

❮ Previous
Next ❯

Citations

Apr 29, 2015·Hormones and Behavior·Elinor L SullivanJeanette C Valleau
Feb 7, 2017·Journal of Chemical Neuroanatomy·Aparna ShekarAurelio Galli
Oct 28, 2015·The Journal of Biological Chemistry·Yang LiWalter Sandtner
Mar 2, 2019·Child: Care, Health and Development·Deirdre U SweetmanHilary Greaney
Jul 17, 2021·Frontiers in Molecular Neuroscience·Elzbieta ZieminskaJerzy W Lazarewicz

❮ Previous
Next ❯

Related Concepts

Related Feeds

Autism

Autism spectrum disorder is associated with challenges with social skills, repetitive behaviors, and often accompanied by sensory sensitivities and medical issues. Here is the latest research on autism.