RasGRPs (guanine-nucleotide-releasing proteins) are exchange factors for membrane-bound GTPases. All RasGRP family members contain C1 domains which, in other proteins, bind DAG (diacylglycerol) and thus mediate the proximal signal-transduction events induced by this lipid second messenger. The presence of C1 domains suggests that all RasGRPs could be regulated by membrane translocation driven by C1-DAG interactions. This has been demonstrated for RasGRP1 and RasGRP3, but has not been tested directly for RasGRP2, RasGRP4alpha and RasGRP4beta. Sequence alignments indicate that all RasGRP C1 domains have the potential to bind DAG. In cells, the isolated C1 domains of RasGRP1, RasGRP3 and RasGRP4alpha co-localize with membranes and relocalize in response to DAG, whereas the C1 domains of RasGRP2 and RasGRP4beta do not. Only the C1 domains of RasGRP1, RasGRP3 and RasGRP4alpha recognize DAG as a ligand within phospholipid vesicles and do so with differential affinities. Other lipid second messengers were screened as ligands for RasGRP C1 domains, but none was found to serve as an alternative to DAG. All of the RasGRP C1 domains bound to vesicles which contained a high concentration of anionic phospholipids, indicating that this could provide a DAG-independent mechanism for membrane binding by C1 domains. This concept was supported by demonstrating that the C1 domain of RasGRP2 could functionally replace the membrane-binding role of the C1 domain within RasGRP1, despite the inability of the RasGRP2 C1 domain to bind DAG. The RasGRP4beta C1 domain was non-functional when inserted into either RasGRP1 or RasGRP4, implying that the alternative splicing which produces this C1 domain eliminates its contribution to membrane binding.

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It is generally accepted that the superimposed hydrostatic pressure increases fracture strain in sheet metal and mode of fracture changes with applying pressure. Void growth is delayed or completely eliminated under pressure and the shear damage mechanism becomes the dominant mode of fracture. In this study, the effect of superimposed hydrostatic pressure on the ductility of sheet metal under tension is investigated using the finite element (FE) method employing the modified Gurson–Tvergaard–Needleman (GTN) model. The shear damage mechanism is considered as an increment in the total void volume fraction and the model is implemented using the VUMAT subroutine in the ABAQUS/Explicit. It is shown that ductility and fracture strain increase significantly by imposing hydrostatic pressure as it suppresses the damage mechanisms of microvoid growth and shear damage. When hydrostatic pressure is applied, it is observed that although the shear damage mechanism is delayed, the shear damage mechanism is dominant over the growth of microvoids. These numerical findings are consistent with those experimental results published in the previous studies about the effect of superimposed hydrostatic pressure on fracture strain. The numerical results clearly show that the dominant mode of failure changes from microvoid growth to shear damage under pressure. Numerical studies in the literature explain the effect of pressure on fracture strain using the conventional GTN model available in the ABAQUS material behavior library when the mode of fracture does not change. However, in this study, the shear modified GTN model is used to understand the effect of pressure on the shear damage mechanism as one of the individual void volume fraction increments and change in mode of fracture is explained numerically.

The effects of cladding layers of rate-sensitive materials on the ductility and fracture strain of compressed rings are numerically investigated by using the finite element method (FEM) and employing the Johnson–Cook (J–C) model. The results show that ductility is governed by the behavior of the material that is located at the ring outer wall regardless of the volume fraction of the core and clad materials. However, as the number of layers increases, this influence becomes less noticeable. Moreover, as barreling increases at the outer wall and decreases at the inner wall, fracture strain increases. Furthermore, the effects of ring shape factor and bonding type of clad and core materials are numerically evaluated. The numerical results show that less force per unit volume is required to fracture narrower rings and that using a noise diffusion pattern at the interface of the materials is more suitable to simulate crack propagation in the compressed rings and functionally graded materials (FGMs). Additionally, delamination has a direct relation to layer thickness and can occur even in the presence of perfect bonding conditions owing to differences among the material and fracture parameters of laminated layers.