Nathan Basisty

PLoS Biology 2020

Open access · CC0

A proteomic atlas of senescence-associated secretomes for aging biomarker development

▲ 1,393

Nature Metabolism 2020

Preprint · OA

Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages

▲ 428

Aging Cell 2014

Open access · CC-BY

Altered proteome turnover and remodeling by short‐term caloric restriction or rapamycin rejuvenate the aging heart

▲ 328

Nature Protocols 2021

Open access · OA

Algorithmic assessment of cellular senescence in experimental and clinical specimens

▲ 198

Journal of Clinical Investigation 2022

Open access · CC-BY

Connecting aging biology and inflammation in the omics era

▲ 194

Biochimica et Biophysica Acta (BBA) - Bioenergetics 2015

Open access · OA

Mitochondrial dysfunction in cardiac aging

▲ 152

Aging 2016

Open access · CC-BY

Rapamycin transiently induces mitochondrial remodeling to reprogram energy metabolism in old hearts

▲ 132

PROTEOMICS 2018

Open access · CC-BY

Protein Turnover in Aging and Longevity

▲ 116

bioRxiv (Cold Spring Harbor Laboratory) 2019

Preprint · CC-BY

A Proteomic Atlas of Senescence-Associated Secretomes for Aging Biomarker Development

▲ 111

Aging Cell 2019

Open access · CC-BY

Rapamycin persistently improves cardiac function in aged, male and female mice, even following cessation of treatment

▲ 104

Aging Cell 2015

Open access · CC-BY

Subacute calorie restriction and rapamycin discordantly alter mouse liver proteome homeostasis and reverse aging effects

▲ 81

PLoS ONE 2011

Open access · CC-BY

Composition and Acidification of the Culture Medium Influences Chronological Aging Similarly in Vineyard and Laboratory Yeast

▲ 76

Expert Review of Proteomics 2020

Open access · CC-BY

The power of proteomics to monitor senescence-associated secretory phenotypes and beyond: toward clinical applications

▲ 73

The Journals of Gerontology Series A 2023

Open access · CC-BY

Proteomic Analysis of the Senescence-Associated Secretory Phenotype: GDF-15, IGFBP-2, and Cystatin-C Are Associated With Multiple Aging Traits

▲ 73

Current Protocols 2021

Open access · CC-BY

Quantitative Proteomic Analysis of the Senescence‐Associated Secretory Phenotype by Data‐Independent Acquisition

▲ 52

Aging Cell 2016

Open access · CC-BY

Mitochondrial‐targeted catalase is good for the old mouse proteome, but not for the young: ‘reverse’ antagonistic pleiotropy?

▲ 41

PROTEOMICS 2019

Open access · CC-BY

Accumulation of “Old Proteins” and the Critical Need for MS‐based Protein Turnover Measurements in Aging and Longevity

▲ 32

Biology 2023

Open access · CC-BY

Translating Senotherapeutic Interventions into the Clinic with Emerging Proteomic Technologies

▲ 15

Cells 2025

Open access · CC-BY

Cellular Models of Aging and Senescence

▲ 15

bioRxiv (Cold Spring Harbor Laboratory) 2025

Preprint · CC-BY

Deep and Quantitative Proteomic Profiling of Low Volume Mouse Serum Across the Lifespan

▲ 1

bioRxiv (Cold Spring Harbor Laboratory) 2024

Preprint · OA

Inhibition of the metalloprotease ADAM19 as a Novel Senomorphic Strategy to Ameliorate gut permeability and senescence markers by modulating senescence-associated secretory phenotype (SASP)

▲ 0

Collaborators

Works in the record

A proteomic atlas of senescence-associated secretomes for aging biomarker development

Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages

Altered proteome turnover and remodeling by short‐term caloric restriction or rapamycin rejuvenate the aging heart

Algorithmic assessment of cellular senescence in experimental and clinical specimens

Connecting aging biology and inflammation in the omics era

Mitochondrial dysfunction in cardiac aging

Rapamycin transiently induces mitochondrial remodeling to reprogram energy metabolism in old hearts

Protein Turnover in Aging and Longevity

A Proteomic Atlas of Senescence-Associated Secretomes for Aging Biomarker Development

Rapamycin persistently improves cardiac function in aged, male and female mice, even following cessation of treatment

Subacute calorie restriction and rapamycin discordantly alter mouse liver proteome homeostasis and reverse aging effects

Composition and Acidification of the Culture Medium Influences Chronological Aging Similarly in Vineyard and Laboratory Yeast

The power of proteomics to monitor senescence-associated secretory phenotypes and beyond: toward clinical applications

Proteomic Analysis of the Senescence-Associated Secretory Phenotype: GDF-15, IGFBP-2, and Cystatin-C Are Associated With Multiple Aging Traits

Quantitative Proteomic Analysis of the Senescence‐Associated Secretory Phenotype by Data‐Independent Acquisition

Mitochondrial‐targeted catalase is good for the old mouse proteome, but not for the young: ‘reverse’ antagonistic pleiotropy?

Accumulation of “Old Proteins” and the Critical Need for MS‐based Protein Turnover Measurements in Aging and Longevity

Translating Senotherapeutic Interventions into the Clinic with Emerging Proteomic Technologies

Cellular Models of Aging and Senescence

Deep and Quantitative Proteomic Profiling of Low Volume Mouse Serum Across the Lifespan

Inhibition of the metalloprotease ADAM19 as a Novel Senomorphic Strategy to Ameliorate gut permeability and senescence markers by modulating senescence-associated secretory phenotype (SASP)