University of Mainz

About: University of Mainz is a education organization based out in Mainz, Rheinland-Pfalz, Germany. It is known for research contribution in the topics: Population & Immune system. The organization has 37673 authors who have published 71163 publications receiving 2497880 citations. The organization is also known as: Johannes Gutenberg-Universität Mainz & Universität Mainz.

Genome-wide association studies identify four ER negative-specific breast cancer risk loci

Abstract: Estrogen receptor (ER)-negative tumors represent 20-30% of all breast cancers, with a higher proportion occurring in younger women and women of African ancestry. The etiology and clinical behavior of ER-negative tumors are different from those of tumors expressing ER (ER positive), including differences in genetic predisposition. To identify susceptibility loci specific to ER-negative disease, we combined in a meta-analysis 3 genome-wide association studies of 4,193 ER-negative breast cancer cases and 35,194 controls with a series of 40 follow-up studies (6,514 cases and 41,455 controls), genotyped using a custom Illumina array, iCOGS, developed by the Collaborative Oncological Gene-environment Study (COGS). SNPs at four loci, 1q32.1 (MDM4, P = 2.1 × 10(-12) and LGR6, P = 1.4 × 10(-8)), 2p24.1 (P = 4.6 × 10(-8)) and 16q12.2 (FTO, P = 4.0 × 10(-8)), were associated with ER-negative but not ER-positive breast cancer (P > 0.05). These findings provide further evidence for distinct etiological pathways associated with invasive ER-positive and ER-negative breast cancers.

Isolation and subsequent analysis of murine lamina propria mononuclear cells from colonic tissue

Abstract: Studies on colonic cells in the lamina propria (LP) of mice are important for understanding the cellular and immune responses in the gut, especially in inflammatory bowel diseases (such as morbus crohn and colitis ulcerosa). This protocol details a method to isolate LP cells and characterize freshly isolated cells by quality control experiments to obtain cells that can be used for further investigations. After different steps of digestion of the tissue using collagenase, DNase and dispase, the resulting cells are purified using Percoll gradient. The success of the isolation can be analyzed by cell viability test (Trypan Blue exclusion test) and by flow cytometric analysis to assess apoptosis. Finally, the isolated cells can be used for further investigations like comparative studies of mRNA expression, cell-proliferation assay or protein analysis. This protocol can be completed within 6-7 h.

Ectodomain shedding of L1 adhesion molecule promotes cell migration by autocrine binding to integrins

Abstract: The L1 adhesion molecule plays an important role in axon guidance and cell migration in the nervous system. L1 is also expressed by many human carcinomas. In addition to cell surface expression, the L1 ectodomain can be released by a metalloproteinase, but the biological function of this process is unknown. Here we demonstrate that membrane-proximal cleavage of L1 can be detected in tumors and in the developing mouse brain. The shedding of L1 involved a disintegrin and metalloproteinase (ADAM)10, as transfection with dominant-negative ADAM10 completely abolishes L1 release. L1-transfected CHO cells (L1-CHO) showed enhanced haptotactic migration on fibronectin and laminin, which was blocked by antibodies to αvβ5 and L1. Migration of L1-CHO cells, but not the basal migration of CHO cells, was blocked by a metalloproteinase inhibitor, indicating a role for L1 shedding in the migration process. CHO and metalloproteinase-inhibited L1-CHO cells were stimulated to migrate by soluble L1-Fc protein. The induction of migration was blocked by αvβ5-specific antibodies and required Arg-Gly-Asp sites in L1. A 150-kD L1 fragment released by plasmin could also stimulate CHO cell migration. We propose that ectodomain-released L1 promotes migration by autocrine/paracrine stimulation via αvβ5. This regulatory loop could be relevant for migratory processes under physiological and pathophysiological conditions.

Relativistic Néel-order fields induced by electrical current in antiferromagnets

Abstract: We predict that a lateral electrical current in antiferromagnets can induce nonequilibrium Neel-order fields, i.e., fields whose sign alternates between the spin sublattices, which can trigger ultrafast spin-axis reorientation. Based on microscopic transport theory calculations we identify staggered current-induced fields analogous to the intraband and to the intrinsic interband spin-orbit fields previously reported in ferromagnets with a broken inversion-symmetry crystal. To illustrate their rich physics and utility, we consider bulk Mn(2)Au with the two spin sublattices forming inversion partners, and a 2D square-lattice antiferromagnet with broken structural inversion symmetry modeled by a Rashba spin-orbit coupling. We propose an antiferromagnetic memory device with electrical writing and reading.