In this study we aimed to generate mouse antibodies against epitopes found on NPCs. We isolated one antibody (NSC-6) and characterized it in detail. Mass spectrometry using human hippocampal tissue revealed the identity of the recognized antigen as BASP1, a signaling protein that plays a key role in neurite outgrowth and plasticity^{14,15,16,17,18,19}, but here, we demonstrate that it might be utilized as a marker of NSCs in the adult brain.

Similar approaches to developing antibodies against mouse embryonic stem cells have been attempted in the past utilizing mice^46,47 and rabbits⁴⁸. Major drawbacks in mice include immune tolerance to mouse embryonic stem cell surface antigens leading to low antibody production, which could be overcome by immunizing rabbits instead. Regardless of the animal used as a host, a significant number of antibodies are typically generated against intracellular epitopes when animals are immunized with whole cells as was observed in our study.

We found that NSC-6-labeled BASP1 localizes to all radial glia at the E12 stage of brain development, while postnatally, it restricts to the neurogenic areas of the mouse brain but not the cortex. This expression pattern contrasts previous study using DAB-based immunolabeling for NAP-22 (BASP1 alias) in the adult rat brain, which demonstrated robust labeling of cerebral cortex²⁷. While we do not know the basis of this difference in immunolabeling of cortex, possibilities include species variations between rat and mouse expression of BASP1, or differences in epitope recognition between the two antibodies used that could yield distinct patterns of immunoreactivity. Indeed, the two commercial BASP1 polyclonal antibodies did not immunolabel NSCs and in general, exhibited poor staining of the mouse brain tissue.

Summary: Boosting the expression of the ABCC1 gene may not only reduce amyloid plaques in the brain, it might also delay the onset of Alzheimer’s disease.

Source: TGen.

Findings of a study by the Translational Genomics Research Institute (TGen), an affiliate of City of Hope, suggest that increasing expression of a gene known as ABCC1 could not only reduce the deposition of a hard plaque in the brain that leads to Alzheimer’s disease, but might also prevent or delay this memory-robbing disease from developing.

New research reveals how cancer cells endure stress and survive. Publishing in Molecular Cell, an international research team identified mechanisms that human and mouse cells use to survive heat shock and resume their original function – and even pass the memory of the experience of stress down to their daughter cells.

Lead author Anniina Vihervaara, Assistant Professor in Gene Technology at KTH Royal Institute of Technology, says the results provide insight into the mechanisms that coordinate transcription in cells, which potentially could make a vital contribution in disease research.

The researchers examined how embryonic fibroblast cells and cancer cells responded when subjected to heat shock at a temperature of 42C, using advanced technology to monitor the process of transcription across genes and their regulatory regions. Heat shock causes acute proteotoxic stress due to misfolding and aggregation of proteins. To adjust and maintain stability, stressed cells reduce protein synthesis and increase expression of chaperones that help other proteins to maintain their correct configuration. The heat shock response and protein misfolding are involved in many diseases, including cancer, Huntington’s and Alzheimer’s.