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Suppression of TGF-β/SMAD signaling by an inner nuclear membrane phosphatase complex

Cytokines of the TGF-β superfamily control essential cell fate decisions via receptor regulated SMAD (R-SMAD) transcription factors. Ligand-induced R-SMAD phosphorylation in the cytosol triggers their activation and nuclear accumulation. We determine how R-SMADs are inactivated by dephosphorylation in the cell nucleus to counteract signaling by TGF-β superfamily ligands. 

From Local to Systemic: The Journey of Tick Bite Biomarkers in Australian Patients

Tick bites and tick-related diseases are on the rise. Diagnostic tests that identify well-characterised tick-borne pathogens (TBPs) possess limited capacity to address the causation of symptoms associated with poorly characterised tick-related illnesses, such as debilitating symptom complexes attributed to ticks (DSCATT) in Australia. Identification of local signals in tick-bitten skin that can be detected systemically in blood would have both clinical (diagnostic or prognostic) and research (mechanistic insight) utility, as a blood sample is more readily obtainable than tissue biopsies.

A complete genome of an obligately lytic Pseudomonas aeruginosa bacteriophage, Minga-mokiny 4

We report the isolation of a bacteriophage with obligately lytic activity against Pseudomonas aeruginosa from wastewater. The reported phage, Minga-mokiny 4, appears to belong to the Schitoviridae family, is of the Litunavirus genus, and has a 72,362-bp genome. No known genes associated with lysogeny, bacterial resistance, or virulence were predicted.

Neurodevelopmental impairment in children with Robin sequence: A systematic review and meta-analysis

Estimate the global prevalence of neurodevelopmental impairment in children with Robin sequence (RS) at one year or more of age.

Profiling epithelial viral receptor expression in amniotic membrane and nasal epithelial cells at birth

Children with wheeze and asthma present with airway epithelial vulnerabilities, such as impaired responses to viral infection. It is postulated that the in utero environment may contribute to the development of airway epithelial vulnerabilities.