ORCID Profile
0000-0001-7075-0067
Current Organisation
Ludwig-Maximilians-Universitat Munchen
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Springer Science and Business Media LLC
Date: 20-03-2011
Abstract: Leg weakness issues are a great concern for the pig breeding industry, especially with regard to animal welfare. Traits associated with leg weakness are partly influenced by the genetic background of the animals but the genetic basis of these traits is not yet fully understood. The aim of this study was to identify quantitative trait loci (QTL) affecting leg weakness in pigs. Three hundred and ten F 2 pigs from a Duroc × Pietrain resource population were genotyped using 82 genetic markers. Front and rear legs and feet scores were based on the standard scoring system. Osteochondrosis lesions were examined histologically at the head and the condylus medialis of the left femur and humerus. Bone mineral density, bone mineral content and bone mineral area were measured in the whole ulna and radius bones using dual energy X-ray absorptiometry. A line-cross model was applied to determine QTL regions associated with leg weakness using the QTL Express software. Eleven QTL affecting leg weakness were identified on eight autosomes. All QTL reached the 5% chromosome-wide significance level. Three QTL were associated with osteochondrosis on the humerus end, two with the fore feet score and two with the rear leg score. QTL on SSC2 and SSC3 influencing bone mineral content and bone mineral density, respectively, reached the 5% genome-wide significance level. Our results confirm previous studies and provide information on new QTL associated with leg weakness in pigs. These results contribute towards a better understanding of the genetic background of leg weakness in pigs.
Publisher: Springer Science and Business Media LLC
Date: 08-07-2011
DOI: 10.1007/S11033-011-1168-5
Abstract: The present study was aimed to determine the association between metalloproteinase 3 (MMP3), transforming growth factor beta 1 (TGFβ1) and collagen type X alpha I (COL10A1) gene polymorphisms with traits related to leg weakness in pigs. Three hundred Duroc × Pietrain cross breds (DuPi) and 299 pigs of a commercial population (CP) were used for the experiment. DuPi animals were examined for 10 different traits describing leg and feet structure, osteochondrosis (OC) scores and bone density status. Data of OC score at condylus medialis humeri, condylus medialis femoris and distal epiphysis ulna regions of CP were used for association analysis. Significant association (P T) with OC at head of femur and bone mineral density in the DuPi population. Association (P A) with rear leg score and the principle component denoting both OC and feet and leg scores in the DuPi population. No association was found between COL10A1 (g.72 C>T) and leg weakness related traits. The associations of SNPs with OC traits could not be confirmed in the commercial population. Expression analysis of the three candidate genes was performed to compare between healthy and OC. TGFβ1 was found to be highly expressed (P < 0.05) in the OC compared to healthy cartilages, but no significant different expressions were observed for MMP3 and COL10A1 genes. The present finding suggested that TGFβ1 and MMP3 genes variants have an effect on some of the leg weakness related traits.
Publisher: Frontiers Media SA
Date: 10-03-2022
DOI: 10.3389/FMOLB.2022.835302
Abstract: The mitochondrial outer membrane (MOM)-anchored GTPase Miro1, is a central player in mitochondrial transport and homeostasis. The dysregulation of Miro1 in amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD) suggests that Miro1 may be a potential biomarker or drug target in neuronal disorders. However, the molecular functionality of Miro1 under (patho-) physiological conditions is poorly known. For a more comprehensive understanding of the molecular functions of Miro1, we have developed Miro1-specific nanobodies (Nbs) as novel research tools. We identified seven Nbs that bind either the N- or C-terminal GTPase domain of Miro1 and demonstrate their application as research tools for proteomic and imaging approaches. To visualize the dynamics of Miro1 in real time, we selected intracellularly functional Nbs, which we reformatted into chromobodies (Cbs) for time-lapse imaging of Miro1. By genetic fusion to an Fbox domain, these Nbs were further converted into Miro1-specific degrons and applied for targeted degradation of Miro1 in live cells. In summary, this study presents a collection of novel Nbs that serve as a toolkit for advanced biochemical and intracellular studies and modulations of Miro1, thereby contributing to the understanding of the functional role of Miro1 in disease-derived model systems.
Publisher: Frontiers Media SA
Date: 09-12-2021
DOI: 10.3389/FIMMU.2021.799910
Abstract: The advancement of new immunotherapies necessitates appropriate probes to monitor the presence and distribution of distinct immune cell populations. Considering the key role of CD4 + cells in regulating immunological processes, we generated novel single-domain antibodies [nanobodies (Nbs)] that specifically recognize human CD4. After in-depth analysis of their binding properties, recognized epitopes, and effects on T-cell proliferation, activation, and cytokine release, we selected CD4-specific Nbs that did not interfere with crucial T-cell processes in vitro and converted them into immune tracers for noninvasive molecular imaging. By optical imaging, we demonstrated the ability of a high-affinity CD4-Nb to specifically visualize CD4 + cells in vivo using a xenograft model. Furthermore, quantitative high-resolution immune positron emission tomography (immunoPET)/MR of a human CD4 knock-in mouse model showed rapid accumulation of 64 Cu-radiolabeled CD4-Nb1 in CD4 + T cell-rich tissues. We propose that the CD4-Nbs presented here could serve as versatile probes for stratifying patients and monitoring in idual immune responses during personalized immunotherapy in both cancer and inflammatory diseases.
Publisher: EMBO
Date: 27-04-2021
Publisher: Elsevier BV
Date: 07-2010
DOI: 10.1016/J.GENE.2010.03.009
Abstract: Osteochondrosis (OC) or leg weakness is an economically important disease of young fast growing pigs and is a concern of animal welfare. The etiology and pathogenesis of osteochondrosis is not fully understood yet, but any abnormalities in the formation of hypertrophic chondrocytes and disrupted blood supply to the growth cartilage are very important predisposing factors. Matrix gla protein (MGP) as a potential calcification inhibitor of extracellular matrix might contribute to the development of OC. Molecular characterization, polymorphisms analysis, methylation at promoter region and expression of MGP gene and protein were performed in both healthy and OC cartilage collected from a DurocxPietrain resource population. The porcine MGP gene consists of 4 exons and 3 introns. The full-length MGP cDNA isolated from articular cartilage consists of 606 bp with a 69-bp 5' UTR, a 312-bp open reading frame with a start codon, a 225-bp 3' UTR. Three single-nucleotide polymorphisms (SNP) were detected in the intron 1 (A-115G, C-1073T and C-1135A) and one in the 3'UTR (C-3767T). The relative abundance of MGP mRNA was lower (P<0.05) in OC compared with healthy cartilage. Moreover, the intensity of MGP band was lower (P<0.05) in OC group when quantified by western blot. Furthermore, one CpG region was identified in MGP promoter and DNA methylation of three CG sites were higher in OC compared with normal cartilage. This suggested that the high DNA methylation at specific CG sites in the MGP promoter might be involved in the down regulation of MGP in OC. Immunofluorescence of normal cartilage collected from pigs of different ages revealed that MGP signals were higher in younger pigs and decreased in the older pigs. The MGP protein was expressed more near to the cartilage canals. These results suggest that the MGP gene might be a potential candidate gene for the development of OC in pigs.
Location: United States of America
No related grants have been discovered for Armin Manfred Scholz.