165 research outputs found
More than skin deep: Functional genomic basis for resistance to Amphibian Chytridiomycosis
The amphibian-killing chytrid fungus Batrachochytriumdendrobatidis (Bd) is one of themost generalist pathogens known, capable of
infecting hundreds of species globally and causing widespread population declines and extinctions. However, some host species are
seemingly unaffected by Bd, tolerating or clearing infections without clinical signs of disease. Variation in host immune responses is
commonly evoked for these resistant or tolerant species, yet to date,we have nodirect comparisonof amphibian species responses to
infection at the level of gene expression. In this study,we challenged four CentralAmerican frog species that vary in Bd susceptibility,
with a sympatric virulent strain of the pathogen. We compared skin and spleen orthologous gene expression using differential
expression tests and coexpression gene network analyses.Wefound that resistant species have reduced skin inflammatory responses
andincreased expressionofgenes involved inskin integrity. Incontrast, onlyhighly susceptible species exhibited suppressionof splenic
T-cell genes. We conclude that resistance to chytridiomycosis may be related to a speciesβ ability to escape the immunosuppressive
activity of the fungus. Moreover, our results indicate that within-species differences in splenic proteolytic enzyme gene expression
may contribute to intraspecific variation in survival. This first comparison of amphibian functional immunogenomic architecture in
response to Bd provides insights into key genetic mechanisms underlying variation in disease outcomes among amphibian species
Determination of from quenched and dynamical QCD
The scale parameter is computed on the lattice in
the quenched approximation and for flavors of light dynamical quarks.
The dynamical calculation is done with non-perturbatively improved
Wilson fermions. In the continuum limit we obtain
MeV and
MeV, respectively.Comment: 16 pages, 6 figures. Minor changes. Final version to be published in
Phys. Lett.
Non-perturbative Landau gauge and infrared critical exponents in QCD
We discuss Faddeev-Popov quantization at the non-perturbative level and show
that Gribov's prescription of cutting off the functional integral at the Gribov
horizon does not change the Schwinger-Dyson equations, but rather resolves an
ambiguity in the solution of these equations. We note that Gribov's
prescription is not exact, and we therefore turn to the method of stochastic
quantization in its time-independent formulation, and recall the proof that it
is correct at the non-perturbative level. The non-perturbative Landau gauge is
derived as a limiting case, and it is found that it yields the Faddeev-Popov
method in Landau gauge with a cut-off at the Gribov horizon, plus a novel term
that corrects for over-counting of Gribov copies inside the Gribov horizon.
Non-perturbative but truncated coupled Schwinger-Dyson equations for the gluon
and ghost propagators and in Landau gauge are solved
asymptotically in the infrared region. The infrared critical exponents or
anomalous dimensions, defined by and are obtained in space-time dimensions . Two
possible solutions are obtained with the values, in dimensions, , or .Comment: 26 pages. Modified 2.25.02 to update references and to clarify
Introduction and Conclusio
The E3 ubiquitin ligase TRIM25 regulates adipocyte differentiation via proteasomemediated degradation of PPAR gamma
Peroxisome proliferator-activated receptor gamma (PPAR??) is a ligand-dependent transcription factor that regulates adipocyte differentiation and glucose homeostasis. The transcriptional activity of PPAR?? is regulated not only by ligands but also by post-translational modifications (PTMs). In this study, we demonstrate that a novel E3 ligase of PPAR??, tripartite motif-containing 25 (TRIM25), directly induced the ubiquitination of PPAR??, leading to its proteasome-dependent degradation. During adipocyte differentiation, both TRIM25 mRNA and protein expression significantly decreased and negatively correlated with the expression of PPAR??. The stable expression of TRIM25 reduced PPAR?? protein levels and suppressed adipocyte differentiation in 3T3-L1 cells. In contrast, the specific knockdown of TRIM25 increased PPAR?? protein levels and stimulated adipocyte differentiation. Furthermore, TRIM25-knockout mouse embryonic fibroblasts (MEFs) exhibited an increased adipocyte differentiation capability compared with wild-type MEFs. Taken together, these data indicate that TRIM25 is a novel E3 ubiquitin ligase of PPAR?? and that TRIM25 is a novel target for PPAR??-associated metabolic diseases
SS18 Together with Animal-Specific Factors Defines Human BAF-Type SWI/SNF Complexes
Contains fulltext :
94049.pdf (publisher's version ) (Open Access
Advances in estrogen receptor biology: prospects for improvements in targeted breast cancer therapy
Estrogen receptor (ER) has a crucial role in normal breast development and is expressed in the most common breast cancer subtypes. Importantly, its expression is very highly predictive for response to endocrine therapy. Current endocrine therapies for ER-positive breast cancers target ER function at multiple levels. These include targeting the level of estrogen, blocking estrogen action at the ER, and decreasing ER levels. However, the ultimate effectiveness of therapy is limited by either intrinsic or acquired resistance. Identifying the factors and pathways responsible for sensitivity and resistance remains a challenge in improving the treatment of breast cancer. With a better understanding of coordinated action of ER, its coregulatory factors, and the influence of other intracellular signaling cascades, improvements in breast cancer therapy are emerging
- β¦