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Medicine

D-Index
77
Citations
26805
World Ranking
18306
National Ranking
9135

Overview

Martin R. Pollak is affiliated with the Beth Israel Deaconess Medical Center in the United States. Their research spans multiple domains within medicine, with a significant focus on nephrology, genetics, and molecular biology.

The primary fields of study for Martin R. Pollak include:

  • Medicine
  • Biochemistry, Genetics and Molecular Biology

Within these broader fields, research has concentrated on subfields such as:

  • Nephrology
  • Genetics
  • Molecular Biology
  • Gastroenterology
  • Pulmonary and Respiratory Medicine

The main topics of their work cover various aspects of renal and related diseases:

  • Renal Diseases and Glomerulopathies
  • Chronic Kidney Disease and Diabetes
  • Renal and related cancers
  • Chronic Lymphocytic Leukemia Research
  • Celiac Disease Research and Management
  • Genetic and Kidney Cyst Diseases
  • Amyloidosis: Diagnosis, Treatment, Outcomes

Martin R. Pollak has contributed to numerous scientific publications. Prominent publication venues include:

  • Journal of the American Society of Nephrology
  • bioRxiv (Cold Spring Harbor Laboratory)
  • Journal of Cystic Fibrosis
  • Kidney International
  • Kidney360

Frequent co-authors in their research efforts have been:

  • David J. Friedman
  • Rasheed Gbadegesin
  • Matthias Kretzler
  • Simone Sanna-Cherchi
  • Ali G. Gharavi

Recent papers reflecting their research interests include the following:

  • APOL1 Nephropathy: From Genetics to Clinical Applications, 2020, Clinical Journal of the American Society of Nephrology
  • Inaxaplin for Proteinuric Kidney Disease in Persons with Two APOL1 Variants, 2023, New England Journal of Medicine
  • Genetics in chronic kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference, 2022, Kidney International
  • Kidney Disease-Associated APOL1 Variants Have Dose-Dependent, Dominant Toxic Gain-of-Function, 2020, Journal of the American Society of Nephrology
  • Aberrantly glycosylated IgG elicits pathogenic signaling in podocytes and signifies lupus nephritis, 2021, JCI Insight

Best Publications

  • Association of trypanolytic ApoL1 variants with kidney disease in African Americans.

    Giulio Genovese;Giulio Genovese;David J. Friedman;Michael D. Ross;Laurence Lecordier

  • Mutations in ACTN4, encoding alpha-actinin-4, cause familial focal segmental glomerulosclerosis.

    Joshua M. Kaplan;Sung Han Kim;Kathryn N. North;Helmut Rennke

  • TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function.

    Jochen Reiser;Krishna R Polu;Clemens C Möller;Peter Kenlan

  • Mutations in the human Ca2+-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism

    Martin R. Pollak;Edward M. Brown;Yah-Huei Wu Chou;Steven C. Hebert

  • Stem cell engraftment at the endosteal niche is specified by the calcium-sensing receptor

    Gregor B. Adams;Karissa T. Chabner;Ian R. Alley;Douglas P. Olson

  • APOL1 Genetic Variants in Focal Segmental Glomerulosclerosis and HIV-Associated Nephropathy

    Jeffrey B. Kopp;George W. Nelson;Karmini Sampath;Randall C. Johnson;Randall C. Johnson

  • A mouse model of human familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism

    Chrystal Ho;David A. Conner;Martin R. Pollak;Martin R. Pollak;Daniel J. Ladd;Daniel J. Ladd

  • Autosomal dominant hypocalcaemia caused by a Ca 2+ -sensing receptor gene mutation

    Martin R. Pollak;Edward M. Brown;Herschel L. Estep;Peter N. McLaine

  • Expression and Characterization of Inactivating and Activating Mutations in the Human Ca2+o-sensing Receptor

    Mei Bai;Steven Quinn;Sunita Trivedi;Olga Kifor

  • Mutations in the formin gene INF2 cause focal segmental glomerulosclerosis

    Elizabeth J Brown;Johannes S Schlöndorff;Johannes S Schlöndorff;Daniel J Becker;Daniel J Becker;Hiroyasu Tsukaguchi;Hiroyasu Tsukaguchi;Hiroyasu Tsukaguchi

  • Research capacity. Enabling the genomic revolution in Africa

    Charles Rotimi;Akin Abayomi;Alash'le Abimiku;Victoria May Adabayeri

  • ADCK4 mutations promote steroid-resistant nephrotic syndrome through CoQ10 biosynthesis disruption

    Shazia Ashraf;Heon Yung Gee;Stephanie Woerner;Stephanie Woerner;Letian X. Xie

  • Mice deficient in α-actinin-4 have severe glomerular disease

    Claudine H. Kos;Tu Cam Le;Sumita Sinha;Joel M. Henderson

  • Mutations causing medullary cystic kidney disease type 1 lie in a large VNTR in MUC1 missed by massively parallel sequencing

    Andrew Kirby;Andreas Gnirke;David B Jaffe;Veronika Barešová

  • Calcium-Ion–Sensing Cell-Surface Receptors

    Edward M. Brown;Martin Pollak;Christine E. Seidman;J.G. Seidman

  • Innate immunity pathways regulate the nephropathy gene Apolipoprotein L1.

    Brendan Nichols;Prachi Jog;Jessica H. Lee;Daniel Blackler

  • NPHS2 mutations in late-onset focal segmental glomerulosclerosis: R229Q is a common disease-associated allele

    Hiroyasu Tsukaguchi;Akulapalli Sudhakar;Tu Cam Le;Trang Nguyen

  • The Extracellular Calcium-Sensing Receptor: Its Role in Health and Disease

    Edward M. Brown;Martin Pollak;Steven C. Hebert

  • Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis.

    Shreeram Akilesh;Hani Suleiman;Haiyang Yu;M. Christine Stander

  • Association of Trypanolytic ApoL1 Variants with Kidney Disease in

    Giulio Genovese;David J. Friedman;Michael D. Ross

Frequent Co-Authors

Edward M. Brown
Edward M. Brown University of Rochester Medical Center
Seth L. Alper
Seth L. Alper Beth Israel Deaconess Medical Center
Giulio Genovese
Giulio Genovese Broad Institute
Christine E. Seidman
Christine E. Seidman Harvard University
Steven C. Hebert
Steven C. Hebert Yale University
Jeffrey B. Kopp
Jeffrey B. Kopp National Institutes of Health
David B. Mount
David B. Mount Brigham and Women's Hospital
David Goltzman
David Goltzman McGill University
Friedhelm Hildebrandt
Friedhelm Hildebrandt Boston Children's Hospital
David A. Weitz
David A. Weitz Harvard University

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