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发帖数: 240 | 1 Josef Martin Penninger
Most significant scientific contributions:
Our basic approach is to genetically manipulate and change genes in mice and
to
determine the effects of these mutations in development of the whole
organism and in
diseases. From these mutations we are trying to establish basic principles
of
development and basic mechanisms of disease pathogenesis. My laboratory
focuses on
heart diseases, autoimmune diseases and cancers, and bone diseases. On all
the listed
contributions below I am the principal investigator who coordinated the
research and
came up with the ideas. I have published more than 360 papers (312 listed on
Pubmed),
gave more than 450 public talks on science, and was listed twice top 10 in
world for most
cited scientists in all fields of science (ISI). H-index: 74 (Google Scholar
).
(1995) Identification of a cell population in our body that spontaneously
kills tumor
cells as a proof of immunosurveillance in vivo [Penninger et al. Nature]
(1997) Identification of the genetic principle how cells can sense stress [
Nishina et
al. Nature].
(1998) Identification of a molecular motor (Vav1) that allows cells to
cluster the
antigen receptor [Fischer et al. Curr. Biol. 1998; Kong et al. J. Exp. Med.
1998;
Penninger and Crabtree, Cell 1999].
(1999) First genetic proof that OPGL is the critical regulator for
osteoclasts that
controls bone loss in old age osteoporosis, cancer metastases, tooth loss,
or
arthritis [Kong et al. Nature, 1999].
(1999) First molecular explanation why children with acute leukemias, and
patients
suffering from people with leukemias, melanomas, breast cancers or prostate
cancers, asthma, chronic infections (AIDS, hepatitis, tuberculosis),
diabetes or
multiple sclerosis suffer bone loss. We also identified the molecular
principle of
bone loss and cartilage loss in arthritis. Inhibition of the osteoporosis
gene OPGL
completely prevents bone loss associated with these diseases in animal
models
and completely prevents clinical symptoms and crippling in arthritis. Based
on
these findings, drugs are being developed to block bone loss in all of these
diseases. These drugs act like insulin for diabetes, but in this case for
all types of
bone loss. [Kong et a, Nature, 1999].
(1999) Identification of first causal link between bacterial infections and
heart
disease. [Bachmaier et al. Science 1999].
(2000) Identification of (Cbl-b) as the first E3 ligase that controls T cell
activation
and T cell tolerance. [Bachmaier et al. Nature 2000; Krawczyk et al.
Immunity,
2000]
(2000) Elucidation of the role of PI3K in T cell and neutrophil
functions [Sasaki et
al. Science 2000].
(2000) First molecular and evolutionary explanation for gender bias and sex
hormone regulation of bone loss in females [Fata et al. Cell, 2000].
(2000) First paper to show that OPGL regulates tooth loss and that
inhibition of
this pathway can completely prevent loss of teeth [Teng et al. J. Clin.
Invest.].
(2001) Genetic identification of a second mitochondrial-regulated,
caspaseindependent
pathway that controls the first wave of programmed cell death during
mouse morphogenesis. [Susin et al. Nature 1999; Joza et al. Nature 2001].
(2002) Identification of the central role of the DREAM gene in pain
perception and
a novel paradigm in pain research [Cheng et la. Cell 2002].
(2002) Identification of ACE2 as a novel heart failure gene. Loss of ACE2
results
in an animal model that mimics human coronary heart disease [Crackower et al.
Nature 2002].
(2002) Elucidation of two distinct PI3K signaling patways that control heart
muscle
cell size and heart muscle function [Crackower et al. Cell 2002].
(2003) Identification of Carma1/CRD11 as essential molecule in T cell
activation
and antigen receptor induced NfKB activation
(2003) Identification of a gene that regulates male specific fertility and
is required
for chromosomes in sperm cells to find their right partners [Crackower et al.
Science 2003].
(2003) Elucidation of cooperation between adaptive and innate immunity that
is
required by dendritic cell-induced autoimmune heart failure [Eriksson et al.
Nature
Medicine 2003].
(2004) Identification of the important role of Stress Kinase MKK7 in G2/M
cellcycle
progression and cellular senescence [Wada et al. Nature Cell Biol. 2004].
(2004) Identification of the essential role of the E3 ubiquitin ligase Cbl-b
in T cell
anergy induction [Jeon et al. Immunity. 2004].
(2004) Elucidation of dexras1 potentiates photic and suppresses non-photic
responses of the circadian clock. [Cheng et al. Neuron. 2004].
(2005) Identification of the molecular scaffold Gab2 as a crucial component
of
RANK signaling and osteoclastogenesis [Wada et al. Nature Medicine. 2005].
(2005) Identification of the SARS-coronavirus receptor ACE2 as a crucial
factor in
SARS pathogenesis [Kuba et al. Nature Medicine. 2005].
(2005) First paper to show that ACE2 protects from Severe Acute Lung Failure
[Imai et al. Nature. 2005].
(2006) Identification of a novel soil factor, RANKL/RANK, that could explain
selective cancer metastases to bones [Jones et al. Nature. 2006].
(2006) First identification of genes that control electricity regulated
wound healing
[Zhao et al. Nature. 2006].
(2006) First identification of a novel amino acid transport molecule in the
kidney
with direct connection to diabetes [Danilczyk et al. Nature 2006].
(2007) Identification of an entirely novel tumor suppressor involved in
multiple
cancers [Zhang et al. Nature Medicine 2007].
(2007) Identification of the E3 ligase Cbl-b as a key molecule involved in
tumor
rejection [Loeser et al. J. Exp. Med. 2007].
(2007) First description that primary genetic defects in mitochondrial
OxPhos can
protect from diabetes and obesity [Pospisilik et al. Cell 2007].
(2008) Identification of a common lung injury pathway in bird flu, SARS, or
anthrax [Imai et al. Cell 2008].
(2009) First in vivo whole fly genome screen on innate immunity [Cronin et
al.
Science 2009].
(2009) Identification of RANKL/RANK as central regulators of fever and
female
body temperature [Hanada et al. Nature 2009]
(2010) First whole genome in vivo screen on obesity in Drosophila and
identification of a novel regulator for white and brown fat development in
mammals [Pospisilik et al. Cell 2010].
(2010) First whole genome in vivo screen on heart failure in Drosophila and
identification of CCR4/Not as regulator of heart failure in mice and sudden
cardiac death in humans [Neely et al. Cell 2010]. |
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