Identification of the Human SULT Enzymes Involved in the Metabolism of Rotigotine

Jia, Chaojun; Luo, Lijun; Kurogi, Katsuhisa; Yu, Jiang; Zhou, Chun; Liu, Ming‐Cheh

doi:10.1002/jcph.658

Cited by 5 publications

(2 citation statements)

References 47 publications

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“…The qualitatively identical regulatory effects of pH o on both influx and efflux of SO 4 2− together suggest an allosteric regulatory effect of SO 4 2− transport. In the absence of pH i -sensitive SO 4 2− transport by human SLC26A1, it is not straightforward to link the transporter's pH o sensitivity to alkaline pH-stimulated proteoglycan sulfation [20] or to alkaline pH-stimulated metabolic N-sulfation of drugs [33]. We suggest that aa sequence differences in ecto-loops or elsewhere may explain the opposite pH-sensitivites of human and rodent SLC26A1.…”

Section: Discussionmentioning

confidence: 99%

Extracellular Cl− regulates human SO4 2−/anion exchanger SLC26A1 by altering pH sensitivity of anion transport

Heneghan

Vandorpe

et al. 2016

Pflugers Arch - Eur J Physiol

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Genetic deficiency of the SLC26A1 anion exchanger in mice is known to be associated with hyposulfatemia and hyperoxaluria with nephrolithiasis, but many aspects of human SLC26A1 function remain to be explored. We report here the functional characterization of human SLC26A1, a DIDS-sensitive, electroneutral sodium-independent anion exchanger transporting sulfate, oxalate, bicarbonate, thiosulfate and (with divergent properties) chloride. Human SLC26A1-mediated anion exchange differs from that of its rodent orthologs in its stimulation by alkaline pHo and inhibition by acidic pHo but not pHi, and in its failure to transport glyoxylate. SLC26A1-mediated transport of sulfate and oxalate is highly dependent on allosteric activation by extracellular chloride or nonsubstrate anions. Extracellular chloride stimulates apparent Vmax of human SLC26A1-mediated sulfate uptake by conferring a two-log decrease in sensitivity to inhibition by extracellular protons, without changing transporter affinity for extracellular sulfate. In contrast to SLC26A1-mediated sulfate transport, SLC26A1-associated chloride transport is activated by acid pHo, shows reduced sensitivity to DIDS, and exhibits cation-dependence of its DIDS-insensitive component. Human SLC26A1 resembles SLC26 paralogs in its inhibition by phorbol ester activation of PKC, which differs in its undiminished polypeptide abundance at or near the oocyte surface. Mutation of SLC26A1 residues corresponding to candidate anion binding site-associated residues in avian SLC26A5/prestin altered anion transport in patterns resembling those of prestin. However, rare SLC26A1 polymorphic variants from a patient with renal Fanconi Syndrome and from a patient with nephrolithiasis/calcinosis exhibited no loss-of-function phenotypes consistent with disease pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Extracellular Cl− regulates human SO4 2−/anion exchanger SLC26A1 by altering pH sensitivity of anion transport

Heneghan

Vandorpe

et al. 2016

Pflugers Arch - Eur J Physiol

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“…SULTs are usually dimeric and, thus, have two active sites for 3'- Sulfotransferases belong to a superfamily that consists of 13 human SULT genes that are divided into 4 families: SULT1, SULT2, SULT4, and SULT6 [75,78,79,85,86]. The SULT1 family contains phenol subfamilies: SULT1A1, SULT1A2, SULT1A3, SULT1A4, SULT1B1, SULT1C2, SULT1C3, SULT1C4 and the estrogen SULT, SULT1E1 [36,74,87,88]. The SULT2 family is mainly involved in the sulfation of steroid hormones and sterols.…”

Section: Overviewmentioning

confidence: 99%

The potential disruption of estrogen and androgen homeostasis and adipocyte differentiation by metabolites of common airborne polychlorinated biphenyls

Parker¹

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The potential disruption of estrogen and androgen homeostasis The potential disruption of estrogen and androgen homeostasis and adipocyte differentiation by metabolites of common airborne and adipocyte differentiation by metabolites of common airborne polychlorinated biphenyls polychlorinated biphenylsii To my family iii I can do all things through Christ which strengtheneth me.Philippians 4:13 King James Version iv ACKNOWLEDGEMENTS First and foremost, I would like to thank God for seeing me through this process.He has surrounded me with so many genuine, supportive and caring people that have helped me along this journey. I would also like to express my gratitude to several other individuals that have helped me to achieve various milestones and dreams.I would like to thank Dr. Duffel for accepting me into his lab and for his mentorship and advisement throughout my graduate education. I appreciate the many letters of recommendation that he has written on my behalf and his guidance on my research. With his support and advocacy, I was awarded many fellowships, completed an internship at SC Johnson and Sons, and presented at over 20 conferences that took place in Japan, California, Puerto Rico, and other fascinating places. I appreciate his patience and support during my time in his lab and for the many lessons that I was grateful to learn there. Two important lessons that I learned was to always believe in myself especially when facing adversity and that I can accomplish anything that I set my mind to. My experiences and training during my time in your lab elevated my networking skills, professional network, mentoring style, helped me discover many scientific opportunities and I received many incredible job opportunities spanning from industry and academia upon graduation. I look forward to seeing the new heights that our careers will reach and staying in contact! Thank you again for all that you've done! I would also like to thank my thesis committee members: Dr. Michael Duffel, Dr.

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Consensus Guidelines for Therapeutic Drug Monitoring in Neuropsychopharmacology: Update 2017

Bergemann²,

et al. 2017

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Therapeutic drug monitoring (TDM) is the quantification and interpretation of drug concentrations in blood to optimize pharmacotherapy. It considers the interindividual variability of pharmacokinetics and thus enables personalized pharmacotherapy. In psychiatry and neurology, patient populations that may particularly benefit from TDM are children and adolescents, pregnant women, elderly patients, individuals with intellectual disabilities, patients with substance abuse disorders, forensic psychiatric patients or patients with known or suspected pharmacokinetic abnormalities. Non-response at therapeutic doses, uncertain drug adherence, suboptimal tolerability, or pharmacokinetic drug-drug interactions are typical indications for TDM. However, the potential benefits of TDM to optimize pharmacotherapy can only be obtained if the method is adequately integrated in the clinical treatment process. To supply treating physicians and laboratories with valid information on TDM, the TDM task force of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) issued their first guidelines for TDM in psychiatry in 2004. After an update in 2011, it was time for the next update. Following the new guidelines holds the potential to improve neuropsychopharmacotherapy, accelerate the recovery of many patients, and reduce health care costs.

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Identification of the Human SULT Enzymes Involved in the Metabolism of Rotigotine

Cited by 5 publications

References 47 publications

Extracellular Cl− regulates human SO4 2−/anion exchanger SLC26A1 by altering pH sensitivity of anion transport

Extracellular Cl− regulates human SO4 2−/anion exchanger SLC26A1 by altering pH sensitivity of anion transport

The potential disruption of estrogen and androgen homeostasis and adipocyte differentiation by metabolites of common airborne polychlorinated biphenyls

Consensus Guidelines for Therapeutic Drug Monitoring in Neuropsychopharmacology: Update 2017

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