Skip to main content
Porträt Natalie Krahmer
Helmholtz Munich | ©Michael Haggenmueller

Dr. Natalie Krahmer

Emmy Noether Research Group Leader Cellular Proteomics and Metabolic Signaling, Institute of Diabetes and Obesity
+49 89 3187 43359Email meBuilding/Room: 3620

Academic Career and Research Areas

Natalie is intrigued by the question how chronic overnutritiuon affects the organization and functions of cells and how this contributes to obesity and metabolic disease. Natalie’s lab develops spatial proteomic tools to map the localization and modifications of proteins at large scale and to generate systematic organellar atlases of organs and tissues. Their aim is to combine these unbiased proteomics tools with cell biological and biochemical methods to characterize the reprogramming of signaling, cellular metabolism and organelle functions in metabolic diseases to identify novel drug targets. A particular interest of her lab is to discover factors that drive progression of fatty liver disease and to elucidate how genetic risk factors influence the cellular processes in order to develop pharmaceutical intervention strategies.

Natalie Krahmer entered the metabolic field during her PhD when she focused on the cell biology of lipid storage.  With her work at the Max-Planck Institute of Biochemistry in Munich and during research stays in the US at Yale Medical School and at UCSF, San Francisco, she elucidated the mechanisms of how lipid droplets, the cellular lipid storage depots, expand and regulate their proteome. During her postdoc at the Max-Planck Institute of Biochemistry, she was then trained in proteomics and developed spatial proteomic tools to investigate the changes of cellular organization and metabolic signaling in fatty liver disease.

In 2019, Natalie was awarded the DFG Emmy-Noether fellowship to start an independent research group and she joined the Helmholtz Diabetes center as group leader. Together with her team, Natalie moves state of the art proteomics into the collaborative environment of the Helmholtz Diabetes Center and has established collaborations with the pharmaceutical industry.

Fields of Work and Expertise

Organelle proteomicsMetabolic signalingNAFLDSystems biologyDiabetesCell biologylipid droplets

Professional Background

2011

PhD, Max-Planck Institute of Biochemistry

2013 - 2018

Postdoc, Max-Planck Institute of Biochemistry

2019

Group leader at the Helmholtz Diabetes Center

Honors and Awards

2020
EFSD/Novo Nordisk Future Leader Award
2019
German research foundation (DFG) Emmy-Noether Fellow

Publications

Read more

2022 Scientific Article in Methods in Molecular Biology

Caliskan, Ö.S. ; Massacci, G. ; Krahmer, N. ; Sacco, F.

Phosphoproteomics and organelle proteomics in pancreatic islets.

Over the recent years, mass spectrometry (MS)-based proteomics has undergone dramatic advances in sample preparation, instrumentation, and computational methods. Here, we describe in detail, how a workflow quantifies global protein phosphorylation in pancreatic islets and characterizes intracellular organelle composition on protein level by MS-based proteomics.

2020 Scientific Article in EMBO Journal, The

Cinque, L. ; De Leonibus, C. ; Iavazzo, M. ; Krahmer, N. ; Intartaglia, D. ; Salierno, F.G. ; De Cegli, R. ; Di Malta, C. ; Svelto, M. ; Lanzara, C. ; Maddaluno, M. ; Wanderlingh, L.G. ; Huebner, A.K. ; Cesana, M. ; Bonn, F. ; Polishchuk, E. ; Hübner, C.A. ; Conte, I. ; Dikic, I. ; Mann, M. ; Ballabio, A. ; Sacco, F. ; Grumati, P. ; Settembre, C.

MiT/TFE factors control ER-phagy via transcriptional regulation of FAM134B.

Lysosomal degradation of the endoplasmic reticulum (ER) via autophagy (ER-phagy) is emerging as a critical regulator of cell homeostasis and function. The recent identification ofER-phagy receptors has shed light on the molecular mechanisms underlining this process. However, the signaling pathways regulatingER-phagy in response to cellular needs are still largely unknown. We found that the nutrient responsive transcription factorsTFEBandTFE3-master regulators of lysosomal biogenesis and autophagy-controlER-phagy by inducing the expression of theER-phagy receptorFAM134B. TheTFEB/TFE3-FAM134B axis promotesER-phagy activation upon prolonged starvation. In addition, this pathway is activated in chondrocytes byFGFsignaling, a critical regulator of skeletal growth.FGFsignaling inducesJNK-dependent proteasomal degradation of the insulin receptor substrate 1 (IRS1), which in turn inhibits thePI3K-PKB/Akt-mTORC1 pathway and promotesTFEB/TFE3 nuclear translocation and enhancesFAM134B transcription. Notably,FAM134B is required for protein secretion in chondrocytes, and cartilage growth and bone mineralization in medaka fish. This study identifies a new signaling pathway that allowsER-phagy to respond to both metabolic and developmental cues.

Networks and Affiliations

AMPro Funding Logo

AmPro

Logo Deutsches Zentrum für Diabetesforschung;

DZD Deutsches Zentrum für Diabetesforschung

BATenergy CRC TRR333 Logo

TR333