Institution
University of Tübingen
Education•Tübingen, Germany•
About: University of Tübingen is a education organization based out in Tübingen, Germany. It is known for research contribution in the topics: Population & Immune system. The organization has 40555 authors who have published 84108 publications receiving 3015320 citations. The organization is also known as: Eberhard Karls University & Eberhard-Karls-Universität Tübingen.
Topics: Population, Immune system, Transplantation, Context (language use), Gene
Papers published on a yearly basis
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TL;DR: A peak of genomic amplification on chromosome 3q26.33 found in squamous cell carcinomas of the lung and esophagus contains the transcription factor gene SOX2, which is necessary for normal esophageal squamous development, promotes differentiation and proliferation of basal tracheal cells and cooperates in induction of pluripotent stem cells.
Abstract: Lineage-survival oncogenes are activated by somatic DNA alterations in cancers arising from the cell lineages in which these genes play a role in normal development. Here we show that a peak of genomic amplification on chromosome 3q26.33 found in squamous cell carcinomas (SCCs) of the lung and esophagus contains the transcription factor gene SOX2, which is mutated in hereditary human esophageal malformations, is necessary for normal esophageal squamous development, promotes differentiation and proliferation of basal tracheal cells and cooperates in induction of pluripotent stem cells. SOX2 expression is required for proliferation and anchorage-independent growth of lung and esophageal cell lines, as shown by RNA interference experiments. Furthermore, ectopic expression of SOX2 here cooperated with FOXE1 or FGFR2 to transform immortalized tracheobronchial epithelial cells. SOX2-driven tumors show expression of markers of both squamous differentiation and pluripotency. These characteristics identify SOX2 as a lineage-survival oncogene in lung and esophageal SCC.
887 citations
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TL;DR: In this paper, a review of recent studies of QCD Green's functions and their applications in hadronic physics are reviewed. But the issues of gauge fixing, BRS invariance and positivity are briefly discussed, and evidence for the violation of positivity by quarks and transverse gluons in the covariant gauge is collected.
Abstract: Recent studies of QCD Green's functions and their applications in hadronic physics are reviewed. We briefly discuss the issues of gauge fixing, BRS invariance and positivity. Evidence for the violation of positivity by quarks and transverse gluons in the covariant gauge is collected, and it is argued that this is one manifestation of confinement.
We summarise the derivation of the Dyson-Schwinger equations (DSEs) of QED and QCD. The influence of instantons on DSEs in a 2-dimensional model is mentioned. Solutions for the Green's functions in QED in 2+1 and 3+1 dimensions provide tests of various schemes to truncate DSEs. We discuss possible extensions to QCD and their limitations. Truncation schemes for DSEs of QCD are discussed in the axial gauge and in the Landau gauge. We review the available results from a systematic non-perturbative expansion scheme established for Landau gauge QCD. Comparisons to related lattice results, where available, are presented.
The applications of QCD Green's functions to hadron physics are summarized. Properties of ground state mesons are discussed on the basis of the Bethe-Salpeter equation for quarks and antiquarks. The Goldstone nature of pseudoscalar mesons and mechanisms of diquark confinement are reviewed. We discuss some properties of ground state baryons based on their description as Bethe-Salpeter/Faddeev bound states of quark-diquark correlations in the quantum field theory of confined quarks and gluons.
876 citations
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TL;DR: The discovery that globular actin polymerization liberates myocardin-related transcription factor (MRTF) cofactors induces the nuclear transcription factor serum response factor (SRF) to modulate the expression of genes encoding structural and regulatory effectors of actin dynamics stimulated research to better understand the actin–MRTF–SRF circuit.
Abstract: Numerous physiological and pathological stimuli promote the rearrangement of the actin cytoskeleton, thereby modulating cellular motile functions. Although it seems intuitively obvious that cell motility requires coordinated protein biosynthesis, until recently the linkage between cytoskeletal actin dynamics and correlated gene activities remained unknown. This knowledge gap was filled in part by the discovery that globular actin polymerization liberates myocardin-related transcription factor (MRTF) cofactors, thereby inducing the nuclear transcription factor serum response factor (SRF) to modulate the expression of genes encoding structural and regulatory effectors of actin dynamics. This insight stimulated research to better understand the actin-MRTF-SRF circuit and to identify alternative mechanisms that link cytoskeletal dynamics and genome activity.
875 citations
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TL;DR: There appears to be a balance between tumor replication and cell death for as long as 22 years in dormancy candidates and it is concluded that this is one mechanism underlying tumor dormancy.
Abstract: Purpose: The purpose of this study was to test the hypothesis that circulating tumor cells (CTCs) are present in patients many years after mastectomy without evidence of disease and that these CTCs are shed from persisting tumor in patients with breast cancer dormancy. Experimental Design: We searched for CTCs in 36 dormancy candidate patients and 26 age-matched controls using stringent criteria for cytomorphology, immunophenotype, and aneusomy. Results: Thirteen of 36 dormancy candidates, 7 to 22 years after mastectomy and without evidence of clinical disease, had CTCs, usually on more than one occasion. Only 1 of 26 controls had a possible CTC (no aneusomy). The statistical difference of these two distributions was significant (exact P = 0.0043). The CTCs in patients whose primary breast cancer was just removed had a half-life measured in 1 to 2.4 hours. Conclusions: The CTCs that are dying must be replenished every few hours by replicating tumor cells somewhere in the tissues. Hence, there appears to be a balance between tumor replication and cell death for as long as 22 years in dormancy candidates. We conclude that this is one mechanism underlying tumor dormancy.
872 citations
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TL;DR: It is argued that plant resistance is determined by immune receptors that recognize appropriate ligands to activate defense, the amplitude of which is likely determined by the level required for effective immunity.
Abstract: Typically, pathogen-associated molecular patterns (PAMPs) are considered to be conserved throughout classes of microbes and to contribute to general microbial fitness, whereas effectors are species, race, or strain specific and contribute to pathogen virulence. Both types of molecule can trigger plant immunity, designated PAMP-triggered and effector-triggered immunity (PTI and ETI, respectively). However, not all microbial defense activators conform to the common distinction between PAMPs and effectors. For example, some effectors display wide distribution, while some PAMPs are rather narrowly conserved or contribute to pathogen virulence. As effectors may elicit defense responses and PAMPs may be required for virulence, single components cannot exclusively be referred to by one of the two terms. Therefore, we put forward that the distinction between PAMPs and effectors, between PAMP receptors and resistance proteins, and, therefore, also between PTI and ETI, cannot strictly be maintained. Rather, as illustrated by examples provided here, there is a continuum between PTI and ETI. We argue that plant resistance is determined by immune receptors that recognize appropriate ligands to activate defense, the amplitude of which is likely determined by the level required for effective immunity.
867 citations
Authors
Showing all 41039 results
Name | H-index | Papers | Citations |
---|---|---|---|
John Q. Trojanowski | 226 | 1467 | 213948 |
Lily Yeh Jan | 162 | 467 | 73655 |
Monique M.B. Breteler | 159 | 546 | 93762 |
Wolfgang Wagner | 156 | 2342 | 123391 |
Thomas Meitinger | 155 | 716 | 108491 |
Hermann Brenner | 151 | 1765 | 145655 |
Amartya Sen | 149 | 689 | 141907 |
Bernhard Schölkopf | 148 | 1092 | 149492 |
Niels Birbaumer | 142 | 835 | 77853 |
Detlef Weigel | 142 | 516 | 84670 |
Peter Lang | 140 | 1136 | 98592 |
Marco Colonna | 139 | 512 | 71166 |
António Amorim | 136 | 1477 | 96519 |
Alexis Brice | 135 | 870 | 83466 |
Elias Campo | 135 | 761 | 85160 |