Social networks are frequently used to distract, procrastinate, or cope with stress. We aimed to investigate how (problematic) social-networks use affect stress perception in interaction with different stress recovery conditions. A total of 104 participants were randomly assigned to one of four groups. Three groups underwent a stress induction with subsequent stress recovery via (1) using Facebook, (2) reading magazines, or (3) waiting. Another group (4) waited without stress induction. Stress perception was repeatedly assessed with the State-Trait-Anxiety-Inventory. Facebook use and reading magazines decreased acute stress indicating adaptive coping strategies. Stress-recovery conditions and symptom severity showed significant interactions. Facebook use was not effective for individuals with high symptom severity in contrast to non-digital strategies or for individuals with low symptom severity. The usage of social networks may be an adaptive strategy for coping with stress for some people, it is maladaptive for individuals having a problematic usage.

Depletion of liprin-α1, ERC1 or LL5 scaffolds inhibits extracellular matrix degradation by invasive cells. These proteins co-accumulate near invadosomes in NIH-Src cells, identifying a novel invadosome-associated compartment distinct from the core and adhesion ring of invadosomes. Depletion of either protein perturbs the organization of invadosomes without influencing the recruitment of MT1-MMP metalloprotease. Liprin-α1 is not required for de novo formation of invadosomes after their disassembly by microtubules and Src inhibitors, while its depletion inhibits invadosome motility, thus affecting matrix degradation. Fluorescence recovery after photobleaching shows that the invadosome-associated compartment is dynamic, while correlative light immunoelectron microscopy identifies bona fide membrane-free invadosome-associated regions enriched in liprin-α1, which is virtually excluded from the invadosome core. The results indicate that liprin-α1, LL5 and ERC1 define a novel dynamic membrane-less compartment that regulates matrix degradation by affecting invadosome motility.

ERBB2 is a ligand-less tyrosine kinase receptor expressed at very low levels in normal tissues; when overexpressed, it is involved in malignant transformation and tumorigenesis in several carcinomas. In cancer cells, ERBB2 represents the preferred partner of other members of the ERBB receptor family, leading to stronger oncogenic signals, by promoting both ERK and AKT activation. The identification of the specific signaling downstream of ERBB2 has been impaired by the lack of a ligand and of an efficient way to selectively activate the receptor. In this paper, we found that antibodies (Abs) targeting different epitopes on the ERBB2 extracellular domain foster the activation of ERBB2 homodimers, and surprisingly induce a unique cytostatic signaling cascade promoting an ERK-dependent ERBB2 Thr701 phosphorylation, leading to AKT de-phosphorylation, via PP2A Ser/Thr phosphatases. Furthermore, the immunophilin Cyclophilin A plays a crucial role in this pathway, acting as a negative modulator of AKT de-phosphorylation, possibly by competing with Ser/Thr phosphatases for binding to AKT. Altogether, our data show that Ab recognizing ERBB2 extracellular domain function as receptor agonists, promoting ERBB2 homodimer activation, leading to an anti-proliferative signaling. Thus, the ultimate outcome of ERBB2 activity might depend on the dimerization status: pro-oncogenic in the hetero-, and anti-oncogenic in the homo-dimeric form.

While the use of social media and online-communication applications has become an integral part of everyday life, some individuals suffer from an excessive, uncontrolled use of social media despite experiencing negative consequences. In accordance with neuropsychological models of addiction, we assume the tendency of a social-networks-use disorder to be related to an interplay of predisposing personality traits (e.g., impulsivity), and reductions in cognitive functions (e.g., executive functions, inhibitory control). The current study makes first strides towards examining this interplay. In addition to a newly developed social-networks-specific auditory Go-NoGo paradigm, other neuropsychological paradigms were used. Impulsivity and social-networks-use-disorder symptoms were assessed by standardized questionnaires. The results show that the symptom severity of a social-networks-use disorder is mainly associated with attentional impulsivity. General executive functions and specific inhibitory control of social-networks-related cues have no direct effect on symptom severity. However, moderated regression analyses emphasize that increased symptom severity is associated with higher attentional impulsivity, especially if there are additionally reductions in executive functions or specific inhibitory control. The results complement previous findings and inform future research on social-networks-use disorder. The findings support the applicability of theoretical models of addictive behaviors to the social-networks-use disorder and point to social-networks-related specificities regarding attention-related facets.