Surviving the Survival Narrative Part 1: Internalised Racism and the Limits of Resistance

The concept of internalised racism (IR) has been criticised for its potential utilisation to perpetuate ‘victim blaming’. In describing the racialised subject’s indoctrination to racist beliefs about themselves and/or their group, the concept of IR has been a point of difficulty for scholarship which sustains a hyper-focus on racialised resistance towards structural racism and its effects. Some scholars have highlighted that this hyper-focus on resistance is connected to a political stance which essentialises racialised subjects as always resisting. In this article, I further this argument by demonstrating the limitations within resistance strategies employed by some racialised subjects. I utilise participants’ narratives from a wider study to highlight three forms of limitations (conscious renouncing, inadvertent complicity, and non-resistance) in resisting racist ideology. I then draw on these examples to problematise scholarship that sustain a hyper-focus on resistance, one that may inadvertently foreclose the deeper impact of racism upon the racialised

Genome-Wide Prediction of SH2 Domain Targets Using Structural Information and the FoldX Algorithm

Current experiments likely cover only a fraction of all protein-protein interactions. Here, we developed a method to predict SH2-mediated protein-protein interactions using the structure of SH2-phosphopeptide complexes and the FoldX algorithm. We show that our approach performs similarly to experimentally derived consensus sequences and substitution matrices at predicting known in vitro and in vivo targets of SH2 domains. We use our method to provide a set of high-confidence interactions for human SH2 domains with known structure filtered on secondary structure and phosphorylation state. We validated the predictions using literature-derived SH2 interactions and a probabilistic score obtained from a naive Bayes integration of information on coexpression, conservation of the interaction in other species, shared interaction partners, and functions. We show how our predictions lead to a new hypothesis for the role of SH2 domains in signaling

Genome-wide association meta-analysis highlights light-induced signaling as a driver for refractive error.

Refractive errors, including myopia, are the most frequent eye disorders worldwide and an increasingly common cause of blindness. This genome-wide association meta-analysis in 160,420 participants and replication in 95,505 participants increased the number of established independent signals from 37 to 161 and showed high genetic correlation between Europeans and Asians (>0.78). Expression experiments and comprehensive in silico analyses identified retinal cell physiology and light processing as prominent mechanisms, and also identified functional contributions to refractive-error development in all cell types of the neurosensory retina, retinal pigment epithelium, vascular endothelium and extracellular matrix. Newly identified genes implicate novel mechanisms such as rod-and-cone bipolar synaptic neurotransmission, anterior-segment morphology and angiogenesis. Thirty-one loci resided in or near regions transcribing small RNAs, thus suggesting a role for post-transcriptional regulation. Our results support the notion that refractive errors are caused by a light-dependent retina-to-sclera signaling cascade and delineate potential pathobiological molecular drivers