Author Correction: Single-cell analysis of EphA clustering phenotypes to probe cancer cell heterogeneity.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Two high-yield complementary methods to sort cell populations by their 2D or 3D migration speed.

The potential to migrate is one of the most fundamental functions for various epithelial, mesenchymal, and immune cells. Image analysis of motile cell populations, both primary and cultured, typically reveals an intercellular variability in migration speeds. However, cell migration chromatography, the sorting of large populations of cells based on their migratory characteristics, cannot be easily performed.

Author Correction: Single-cell analysis of EphA clustering phenotypes to probe cancer cell heterogeneity.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Single-cell analysis of EphA clustering phenotypes to probe cancer cell heterogeneity.

The Eph family of receptor tyrosine kinases is crucial for assembly and maintenance of healthy tissues. Dysfunction in Eph signaling is causally associated with cancer progression. In breast cancer cells, dysregulated Eph signaling has been linked to alterations in receptor clustering abilities.

Systems-based approach to examine the cytokine responses in primary mouse lung macrophages infected with low pathogenic avian Influenza virus circulating in South East Asia.

Background: Influenza A virus (IAV) is a major public health concern, being responsible for the death of approximately half a million people each year. Zoonotic transmissions of the virus from swine and avian origin have occurred in the past, and can potentially lead to the emgergence of new IAV stains in future pandemics. Pulmonary macrophages have been implicated in disease severity in the lower airway, and understanding the host response of macrophages infected with avian influenza viruses should provide new therapeutic strategies.

Truncated forms of the PA protein containing only the C-terminal domains are associated with the ribonucleoprotein complex within H1N1 influenza virus particles.

We have examined the expression profile of the influenza virus PA protein in pH1N1/2009 virus-infected cells. Immunoblotting analysis of virus-infected MDCK cells revealed the presence of full-length PA protein from 8 h post-infection, together with the simultaneous appearance of PA protein species of approximately 50, 35/39 and 20/25 kDa (collectively referred to as PA*). PA* was also detected in H1N1/WSN-virus-infected cells, indicating that its presence was not virus-specific, and it was also observed in virus-infected A549 and chick embryo fibroblast (CEF) cells, indicating that its presence was not cell-type-specific.

Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.

The host response to the low pathogenic avian influenza (LPAI) H5N2, H5N3 and H9N2 viruses were examined in A549, MDCK, and CEF cells using a systems-based approach. The H5N2 and H5N3 viruses replicated efficiently in A549 and MDCK cells, while the H9N2 virus replicated least efficiently in these cell types. However, all LPAI viruses exhibited similar and higher replication efficiencies in CEF cells.

Protein analysis of purified respiratory syncytial virus particles reveals an important role for heat shock protein 90 in virus particle assembly.

In this study, we used imaging and proteomics to identify the presence of virus-associated cellular proteins that may play a role in respiratory syncytial virus (RSV) maturation. Fluorescence microscopy of virus-infected cells revealed the presence of virus-induced cytoplasmic inclusion bodies and mature virus particles, the latter appearing as virus filaments. In situ electron tomography suggested that the virus filaments were complex structures that were able to package multiple copies of the virus genome.