Tobias Huber

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Tobias Huber (25 August 1971 in Waldkirch) is a German nephrologist and internist. He is university professor and Director and Chairman of the III. Department of Medicine [1] at the University Medical Center Hamburg-Eppendorf. [2] [3] [4]



Huber studied human medicine in Freiburg, Vienna and Tampa from 1992 until 1999. [5] [6] [7] Following his promotion at the Institute of Physiology in Freiburg, he was medical assistant at the nephrologists unit of the University Hospital Freiburg. From 2003 until 2006 Huber was receiving an Emmy Noether scholarship of the Deutsche Forschungsgemeinschaft [8] and worked as Postdoctoral Fellow at the Department of Immunology and Pathology at Washington University in St. Louis. [9] [10] [11] After his habilitation in 2007, Huber was certified as a specialist in internal medicine and became group leader of an Emmy Noether research group in Freiburg. [11] In 2012 Huber had been elected as Heisenberg Fellow and since 2013 he has been holding a Heisenberg professorship for Medicine and Nephrology at the University Medical Center Freiburg. [5] [6] [7] [8] From 2015- 2017 Huber was Vice Chair of the Department of Medicine IV, Chief of the Division of Chronic Kidney Disease at the University Medical Center Freiburg and furthermore, Co-Director of the Center of Systems Biology (ZBSA). [5] [6] [7] [8] [12] Since April 2017 he is the Director and Chairman of the III. Department of Medicine [1] at the University Medical Center Hamburg-Eppendorf. [2] [3] [4] Huber is a Fellow of the American Society of Nephrology (FASN) [13] and a member of the American Society for Clinical Investigation [9] a member of the Association of American Physicians and a member of the German National Academy of Sciences – Leopoldina.

Scientific contribution

Huber's research focus is to understand the complex signaling networks that regulate the development, maintenance and disease progression of the kidney. [14] [15] [16] [17] [9] [10] [11] His team identified several molecular mechanisms important for renal development, maintenance, ageing and disease of the kidney. [16] [18] [19] [9] [10] [20] More recently his team made novel discoveries regarding the tropism and organ injury caused by SARS-CoV-2 (Puelles et al. NEJM 2020, Braun et al., LANCET 2020, Gross et al., LANCET, 2020).

Related Research Articles

<span class="mw-page-title-main">Glomerulus (kidney)</span> Functional unit of nephron

The glomerulus is a network of small blood vessels (capillaries) known as a tuft, located at the beginning of a nephron in the kidney. Each of the two kidneys contains about one million nephrons. The tuft is structurally supported by the mesangium, composed of intraglomerular mesangial cells. The blood is filtered across the capillary walls of this tuft through the glomerular filtration barrier, which yields its filtrate of water and soluble substances to a cup-like sac known as Bowman's capsule. The filtrate then enters the renal tubule of the nephron.

<span class="mw-page-title-main">Podocyte</span> Type of kidney cell

Podocytes are cells in Bowman's capsule in the kidneys that wrap around capillaries of the glomerulus. Podocytes make up the epithelial lining of Bowman's capsule, the third layer through which filtration of blood takes place. Bowman's capsule filters the blood, retaining large molecules such as proteins while smaller molecules such as water, salts, and sugars are filtered as the first step in the formation of urine. Although various viscera have epithelial layers, the name visceral epithelial cells usually refers specifically to podocytes, which are specialized epithelial cells that reside in the visceral layer of the capsule. One type of specialized epithelial cell is podocalyxin.

<span class="mw-page-title-main">Ubiquitin carboxy-terminal hydrolase L1</span> Protein-coding gene in the species Homo sapiens

Ubiquitin carboxy-terminal hydrolase L1 is a deubiquitinating enzyme.

<span class="mw-page-title-main">Diabetic nephropathy</span> Chronic loss of kidney function

Diabetic nephropathy, also known as diabetic kidney disease, is the chronic loss of kidney function occurring in those with diabetes mellitus. Diabetic nephropathy is the leading causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) globally. The triad of protein leaking into the urine, rising blood pressure with hypertension and then falling renal function is common to many forms of CKD. Protein loss in the urine due to damage of the glomeruli may become massive, and cause a low serum albumin with resulting generalized body swelling (edema) so called nephrotic syndrome. Likewise, the estimated glomerular filtration rate (eGFR) may progressively fall from a normal of over 90 ml/min/1.73m2 to less than 15, at which point the patient is said to have end-stage renal disease. It usually is slowly progressive over years.

<span class="mw-page-title-main">Nephrin</span> Mammalian protein found in Homo sapiens

Nephrin is a protein necessary for the proper functioning of the renal filtration barrier. The renal filtration barrier consists of fenestrated endothelial cells, the glomerular basement membrane, and the podocytes of epithelial cells. Nephrin is a transmembrane protein that is a structural component of the slit diaphragm. They are present on the tips of the podocytes as an intricate mesh and convey strong negative charges which repel protein from crossing into the Bowman's space.

Marilyn Gist Farquhar was a pathologist and cellular biologist, Professor of Cellular and Molecular Medicine and Pathology, as well as the chair of the Department of Cellular and Molecular Medicine at the University of California, San Diego School of Medicine, who previously worked at Yale University from 1973 to 1990. She has won the E. B. Wilson Medal and the FASEB Excellence in Science Award. She was married to Nobel Laureate George Emil Palade from 1970 to his death in 2008. Her research focuses on control of intracellular membrane traffic and the molecular pathogenesis of auto immune kidney diseases. She has yielded a number of discoveries in basic biomedical research including: mechanisms of kidney disease, organization of functions that attach cells to one another, and mechanisms of secretions.

<span class="mw-page-title-main">Neutral and basic amino acid transport protein rBAT</span> Protein-coding gene in the species Homo sapiens

Neutral and basic amino acid transport protein rBAT is a protein that in humans is encoded by the SLC3A1 gene.

<span class="mw-page-title-main">LRP2</span> Mammalian protein found in Homo sapiens

Low density lipoprotein receptor-related protein 2 also known as LRP-2 or megalin is a protein which in humans is encoded by the LRP2 gene.

<span class="mw-page-title-main">NPHS2</span> Protein-coding gene in the species Homo sapiens

Podocin is a protein that in humans is encoded by the NPHS2 gene.

<span class="mw-page-title-main">CD2AP</span> Protein

CD2-associated protein is a protein that in humans is encoded by the CD2AP gene.

<span class="mw-page-title-main">PODXL</span> Protein-coding gene in the species Homo sapiens

Podocalyxin-like protein 1 is a protein that in humans is encoded by the PODXL gene.

<span class="mw-page-title-main">SYNPO</span> Mammalian protein found in Homo sapiens

Synaptopodin is a protein that in humans is encoded by the SYNPO gene.

<span class="mw-page-title-main">PTPRO</span> Protein-coding gene in the species Homo sapiens

Receptor-type tyrosine-protein phosphatase O is an enzyme that in humans is encoded by the PTPRO gene.

<span class="mw-page-title-main">KIRREL</span> Protein-coding gene in the species Homo sapiens

Kin of IRRE-like protein 1, also known as NEPH1, is a protein that in humans is encoded by the KIRREL gene.

<span class="mw-page-title-main">American Society of Nephrology</span> U.S. professional organization

Founded in 1966, the American Society of Nephrology (ASN) is the world's largest professional society devoted to the study of kidney disease. Composed of over 20,000 physicians and scientists, ASN promotes expert patient care, advances medical research, and educates the renal community. ASN also informs policymakers about issues of importance to kidney doctors and their patients.

<span class="mw-page-title-main">KIRREL3</span> Protein-coding gene in the species Homo sapiens

Kin of IRRE-like protein 3 (KIRREL3) also known as kin of irregular chiasm-like protein 3 or NEPH2 is a protein that in humans is encoded by the KIRREL3 gene.

Dendrin is a neural and renal protein whose exact function is still relatively unclear; however, its location in the brain and kidneys is well known as are some of the neural processes it affects. Within the brain, dendrin can be found in neurons and is most notably associated with sleep deprivation. Sleep deprivation causes some areas of the brain dendrin levels to increase, but this increase is insignificant and in total sleep deprivation causes a decrease of the mRNA and protein form of dendrin. Along with two other proteins, MAGI/S-SCAM and α-actinin, dendrin is linked to synaptic plasticity and memory formation in the brain. Nicotine levels have also been shown to have an effect on dendrin expression in the brain. Although unlike sleep deprivation, nicotine increases overall dendrin level. Originally thought to be a brain specific protein, there is now evidence to suggest that dendrin is also found in the kidneys. Dendrin is used to detect glomerulopathy or renal disease, based on its location in the kidneys. Within the kidneys it also works to prevent urinary protein loss. Most studies and information on dendrin pertain specifically to rat or mice brains.

George C. Tsokos is an American immunologist who is a professor of medicine at Harvard Medical School and is the chief at Division of Rheumatology and Clinical Immunology at Beth Israel Deaconess Medical Center; Boston, MA

<span class="mw-page-title-main">Börje Haraldsson</span> Swedish Physician-scientist

Börje Haraldsson is a Swedish Physician-scientist known for his work on kidney disease. He is the Chief Executive Officer at Oncorena AB, and a Professor of Physiology in Sahlgrenska Academy at the University of Gothenburg. He is also a Fellow of the American Society of Transplantation (FAST), and the American Society of Nephrology (FASN).


  1. 1 2 "UKE - Arztprofil - Tobias B. Huber".
  2. 1 2 "UKE - Pressemitteilung - Nierenspezialist aus Freiburg übernimmt Leitung der III. Medizinischen Klinik des UKE".
  3. 1 2 Ärzteblatt, Deutscher Ärzteverlag GmbH, Redaktion Deutsches (12 May 2017). "Aufgaben und Ämter".{{cite web}}: CS1 maint: multiple names: authors list (link)
  4. 1 2 "Nierenspezialist aus Freiburg übernimmt Leitung der III. Medizinischen Klinik des UKE".
  5. 1 2 3 "Prof. Dr. Tobias B. Huber — Freiburg Institute for Advanced Studies – FRIAS".
  6. 1 2 3 "CV Tobias Huber". Huberlab Freiburg.
  7. 1 2 3 "Tobias B. Huber -".
  8. 1 2 3 "DFG - GEPRIS - Professor Dr. Tobias B. Huber".
  9. 1 2 3 4 "The American Society for Clinical Investigation".
  10. 1 2 3 "Young Investigator Attains Recognition for Podocyte Research - Kidney News".
  11. 1 2 3 "Prof. Dr. Tobias B. Huber — Freiburg Institute for Advanced Studies – FRIAS".
  12. "Tobias B. Huber MD". Huberlab Freiburg. Archived from the original on 2016-05-31.
  13. "FASN".
  14. Huber, T. B., Schermer, B., Muller, R. U., Hohne, M., Bartram, M., Calixto, A., Hagmann, H., Reinhardt, C., Koos, F., Kunzelmann, K., Shirokova, E., Krautwurst, D., Harteneck, C., Simons, M., Pavenstadt, H., Kerjaschki, D., Thiele, C., Walz, G., Chalfie, M., and Benzing, T. 2006. Podocin and MEC-2 bind cholesterol to regulate the activity of associated ion channels. Proc Natl Acad Sci U S A 103:17079-86. doi : 10.1073/pnas.0607465103.
  15. Huber, T. B., Kwoh, C., Wu, H., Asanuma, K., Godel, M., Hartleben, B., Blumer, K. J., Miner, J. H., Mundel, P., and Shaw, A. S. 2006. Bigenic mouse models of focal segmental glomerulosclerosis involving pairwise interaction of CD2AP, Fyn, and synaptopodin. J Clin Invest 116:1337-45. doi : 10.1172/jci27400.
  16. 1 2 Grahammer, F., Schell, C., and Huber, T. B. 2013. The podocyte slit diaphragm--from a thin grey line to a complex signalling hub. Nat Rev Nephrol 9:587-98. doi : 10.1038/nrneph.2013.169.
  17. Grahammer, F., Nesterov, V., Ahmed, A., Steinhardt, F., Sandner, L., Arnold, F., Cordts, T., Negrea, S., Bertog, M., Ruegg, M. A., Hall, M. N., Walz, G., Korbmacher, C., Artunc, F., and Huber, T. B. 2016. mTORC2 critically regulates renal potassium handling. J Clin Invest doi : 10.1172/jci80304.
  18. Hartleben, B., Godel, M., Meyer-Schwesinger, C., Liu, S., Ulrich, T., Kobler, S., Wiech, T., Grahammer, F., Arnold, S. J., Lindenmeyer, M. T., Cohen, C. D., Pavenstadt, H., Kerjaschki, D., Mizushima, N., Shaw, A. S., Walz, G., and Huber, T. B. 2010. Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice. J Clin Invest 120:1084-96. doi : 10.1172/jci39492.
  19. Godel, M., Hartleben, B., Herbach, N., Liu, S., Zschiedrich, S., Lu, S., Debreczeni-Mor, A., Lindenmeyer, M. T., Rastaldi, M. P., Hartleben, G., Wiech, T., Fornoni, A., Nelson, R. G., Kretzler, M., Wanke, R., Pavenstadt, H., Kerjaschki, D., Cohen, C. D., Hall, M. N., Ruegg, M. A., Inoki, K., Walz, G., and Huber, T. B. 2011. Role of mTOR in podocyte function and diabetic nephropathy in humans and mice. In Invest 121:2197-209. doi : 10.1172/jci44774.
  20. "BIOSS Member Wins Young Investigator Award 2012". 6 December 2012.