You have been warned: Abusing 5G's Warning and Emergency Systems

The Public Warning System (PWS) is an essential part of cellular networks and a country's civil protection. Warnings can notify users of hazardous events (e.g., floods, earthquakes) and crucial national matters that require immediate attention. PWS attacks disseminating fake warnings or concealing precarious events can have a serious impact, causing fraud, panic, physical harm, or unrest to users within an affected area. In this work, we conduct the first comprehensive investigation of PWS security in 5G networks. We demonstrate five practical attacks that may impact the security of 5G-based Commercial Mobile Alert System (CMAS) as well as Earthquake and Tsunami Warning System (ETWS) alerts. Additional to identifying the vulnerabilities, we investigate two PWS spoofing and three PWS suppression attacks, with or without a man-in-the-middle (MitM) attacker. We discover that MitM-based attacks have more severe impact than their non-MitM counterparts. Our PWS barring attack is an effective technique to eliminate legitimate warning messages. We perform a rigorous analysis of the roaming aspect of the PWS, incl. its potentially secure version, and report the implications of our attacks on other emergency features (e.g., 911 SIP calls). We discuss possible countermeasures and note that eradicating the attacks necessitates a scrupulous reevaluation of the PWS design and a secure implementation

Freaky Leaky SMS: Extracting User Locations by Analyzing SMS Timings

Short Message Service (SMS) remains one of the most popular communication channels since its introduction in 2G cellular networks. In this paper, we demonstrate that merely receiving silent SMS messages regularly opens a stealthy side-channel that allows other regular network users to infer the whereabouts of the SMS recipient. The core idea is that receiving an SMS inevitably generates Delivery Reports whose reception bestows a timing attack vector at the sender. We conducted experiments across various countries, operators, and devices to show that an attacker can deduce the location of an SMS recipient by analyzing timing measurements from typical receiver locations. Our results show that, after training an ML model, the SMS sender can accurately determine multiple locations of the recipient. For example, our model achieves up to 96% accuracy for locations across different countries, and 86% for two locations within Belgium. Due to the way cellular networks are designed, it is difficult to prevent Delivery Reports from being returned to the originator making it challenging to thwart this covert attack without making fundamental changes to the network architecture

Control of neuronal excitation-inhibition balance by BMP-SMAD1 signaling

Throughout life, neuronal networks in the mammalian neocortex maintain a balance of excitation and inhibition which is essential for neuronal computation. Deviations from a balanced state have been linked to neurodevelopmental disorders and severe disruptions result in epilepsy. To maintain balance, neuronal microcircuits composed of excitatory and inhibitory neurons sense alterations in neural activity and adjust neuronal connectivity and function. Here, we identified a signaling pathway in the adult mouse neocortex that is activated in response to elevated neuronal network activity. Over-activation of excitatory neurons is signaled to the network through the elevation of BMP2, a growth factor well-known for its role as morphogen in embryonic development. BMP2 acts on parvalbumin-expressing (PV) interneurons through the transcription factor SMAD1, which controls an array of glutamatergic synapse proteins and components of peri-neuronal nets. PV interneuron-specific impairment of BMP2-SMAD1 signaling is accompanied by a loss of PV cell glutamatergic innervation, underdeveloped peri-neuronal nets, and decreased excitability. Ultimately, this impairment of PV interneuron functional recruitment disrupts cortical excitation - inhibition balance with mice exhibiting spontaneous epileptic seizures. Our findings suggest that developmental morphogen signaling is re-purposed to stabilize cortical networks in the adult mammalian brain

ENTH and ANTH domain proteins participate in AP2-independent clathrin-mediated endocytosis

Clathrin-mediated endocytosis (CME) is a major route of entry into eukaryotic cells. A core of evolutionarily ancient genes encodes many components of this system but much of our mechanistic understanding of CME is derived from a phylogenetically narrow sampling of a few model organisms. In the parasite Trypanosoma brucei, which is distantly related to the better characterised animals and fungi, exceptionally fast endocytic turnover aids its evasion of the host immune system. Although clathrin is absolutely essential for this process, the adaptor protein complex 2 (AP2) has been secondarily lost, suggesting mechanistic divergence. Here, we characterise two phosphoinositide-binding monomeric clathrin adaptors, T. brucei (Tb)EpsinR and TbCALM, which in trypanosomes are represented by single genes, unlike the expansions present in animals and fungi. Depletion of these gene products reveals essential, but partially redundant, activities in CME. Ultrastructural analysis of TbCALM and TbEpsinR double-knockdown cells demonstrated severe defects to clathrin-coated pit formation and morphology associated with a dramatic inhibition of endocytosis. Depletion of TbCALM alone, however, produced a distinct lysosomal segregation phenotype, indicating an additional non-redundant role for this protein. Therefore, TbEpsinR and TbCALM represent ancient phosphoinositide-binding proteins with distinct and vital roles in AP2-independent endocytosis

Caveolae protect endothelial cells from membrane rupture during increased cardiac output.

Caveolae are strikingly abundant in endothelial cells, yet the physiological functions of caveolae in endothelium and other tissues remain incompletely understood. Previous studies suggest a mechanoprotective role, but whether this is relevant under the mechanical forces experienced by endothelial cells in vivo is unclear. In this study we have sought to determine whether endothelial caveolae disassemble under increased hemodynamic forces, and whether caveolae help prevent acute rupture of the plasma membrane under these conditions. Experiments in cultured cells established biochemical assays for disassembly of caveolar protein complexes, and assays for acute loss of plasma membrane integrity. In vivo, we demonstrate that caveolae in endothelial cells of the lung and cardiac muscle disassemble in response to acute increases in cardiac output. Electron microscopy and two-photon imaging reveal that the plasma membrane of microvascular endothelial cells in caveolin 1(-/-) mice is much more susceptible to acute rupture when cardiac output is increased. These data imply that mechanoprotection through disassembly of caveolae is important for endothelial function in vivo