Seth L. Alper

ORCID: 0000-0002-6228-2512
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Ion channel regulation and function
  • Ion Transport and Channel Regulation
  • Erythrocyte Function and Pathophysiology
  • Hemoglobinopathies and Related Disorders
  • Neuroscience and Neuropharmacology Research
  • Pancreatic function and diabetes
  • Renal Diseases and Glomerulopathies
  • Genetic and Kidney Cyst Diseases
  • Neonatal Health and Biochemistry
  • Renal and related cancers
  • Fetal and Pediatric Neurological Disorders
  • Cerebrospinal fluid and hydrocephalus
  • Hearing, Cochlea, Tinnitus, Genetics
  • Drug Transport and Resistance Mechanisms
  • Chronic Kidney Disease and Diabetes
  • Renal function and acid-base balance
  • Cardiac electrophysiology and arrhythmias
  • Blood properties and coagulation
  • Neuroscience of respiration and sleep
  • Dialysis and Renal Disease Management
  • Ion Channels and Receptors
  • Nitric Oxide and Endothelin Effects
  • Biomedical Research and Pathophysiology
  • Iron Metabolism and Disorders
  • Vestibular and auditory disorders

Beth Israel Deaconess Medical Center
2016-2025

Harvard University
2016-2025

Massachusetts Institute of Technology
1989-2025

Center for Vascular Biology Research
2013-2025

Broad Institute
2015-2025

Hadassah Medical Center
2007-2025

Boston University
1995-2023

Oxford University Press (United Kingdom)
2018-2020

RELX Group (United States)
2019

Beaumont Hospital
2018

Transgenic plants overexpressing the vacuolar H(+)-pyrophosphatase are much more resistant to high concentrations of NaCl and water deprivation than isogenic wild-type strains. These transgenic accumulate Na(+) K(+) in their leaf tissue wild type. Moreover, direct measurements on isolated membrane vesicles derived from AVP1 type demonstrate that have enhanced cation uptake. The phenotypes suggest increasing proton gradient results increased solute accumulation retention. Presumably,...

10.1073/pnas.191389398 article EN Proceedings of the National Academy of Sciences 2001-09-25

Overexpression of the Arabidopsis thaliana vacuolar H + -pyrophosphatase ( AVP1 ) confers salt tolerance to salt-sensitive ena1 mutant Saccharomyces cerevisiae . Suppression sensitivity requires two ion transporters, Gef1 Cl − channel and Nhx1 Na /H exchanger. These proteins colocalize prevacuolar compartment yeast are thought be required for optimal acidification this compartment. AtNHX1 , plant homologue exchanger, suppresses some phenotypes nhx1 mutant. Moreover, level mRNA in is...

10.1073/pnas.96.4.1480 article EN Proceedings of the National Academy of Sciences 1999-02-16

Using low-stringency hybridization to the rat brain glucose transporter (GT), a 2489-base-pair cDNA clone was isolated from soleus lambda gt10 library. It encodes 509-amino acid protein whose sequence and predicted membrane structure is very similar those of liver GTs. The muscle GT-like 65% identical in amino GT 52% GT; major differences are NH2- COOH-terminal hydrophilic segments. This mRNA expressed predominately tissues where transport sensitive insulin, including striated muscle,...

10.1073/pnas.86.8.2535 article EN Proceedings of the National Academy of Sciences 1989-04-01

The cellular distributions of the kidney form erythrocyte band 3 chloride/bicarbonate exchanger and vacuolar H+-transporting ATPase were examined in rat collecting duct by immunocytochemical staining adjacent semithin sections. Polyclonal anti-peptide antibodies directed against two regions murine erythroid gave a pattern basolateral labeling similar to that seen with entire protein. In medullary almost all intercalated cells expressed membrane displayed apical H+-ATPase. cortical connecting...

10.1073/pnas.86.14.5429 article EN Proceedings of the National Academy of Sciences 1989-07-01

We have investigated the interaction of clotrimazole (CLT) and related compounds with erythroid Ca(2+)-activated K+ channel, a mediator sickle cell dehydration. measured transport, membrane potential, volume upon activation this pathway in erythrocytes. CLT blocked almost completely transport homozygous hemoglobin S cells, IC50 values 29 +/- 15 nM isotonic 20 mM salt solution 51 normal saline (n = 3). The inhibition by was caused specific channel human red since it displaced bound...

10.1172/jci116597 article EN Journal of Clinical Investigation 1993-07-01

Significance People of recent African ancestry develop chronic kidney disease and end stage failure at rates five times that European-Americans. Two coding variants in the apolipoprotein-L1 (APOL1) gene account for nearly all this excess risk. The mechanisms by which APOL1 cause are not understood. Recent evidence suggests transports cations, including K + , across lipid bilayers. Here, we show tetracycline-induced expression risk T-REx-293 cells causes significant net efflux intracellular...

10.1073/pnas.1522913113 article EN Proceedings of the National Academy of Sciences 2015-12-23

Significance African trypanosomes are parasites that can cause sleeping sickness in humans. Humans and some primates, but not other mammals, have a gene called APOL1 protects against certain trypanosomes. Genetic variants arose Africa strongly associated with kidney disease Americans. These disease-associated may risen to high frequency because they defend humans particularly pathogenic trypanosome. In this paper, we show how has evolved by analyzing the distribution of these then...

10.1073/pnas.1400699111 article EN Proceedings of the National Academy of Sciences 2014-05-07

Pathologic water loss from sickle erythrocytes concentrates the abnormal hemoglobin and promotes sickling. The Ca2+-activated K+ channel (Gardos channel) contributes to this deleterious dehydration in vitro, blockade of via could be a potential therapy vivo. We treated five subjects who have cell anemia with oral clotrimazole, specific Gardos inhibitor. Patients were started on dose 10 mg clotrimazole/kg/d for one week. Protocol design allowed daily escalated by mg/kg each week until...

10.1172/jci118537 article EN Journal of Clinical Investigation 1996-03-01
Coming Soon ...