Research roundup: see our neuroscience products in action

Our antibodies are used in cutting-edge neuroscience research around the world. All our neuroscience products are highly validated and created using a unique antigen design for optimal specificity, affinity-purified using the immunogen, and manufactured using a standardized production process to ensure the highest quality. Let's take a look at three recent studies showing our neuroscience products in action.

1) Disruption of endoplasmic reticulum-mitochondria tethering proteins in post-mortem Alzheimer's disease brain (Lau et al. 2020)

Organelle-organelle communication between the endoplasmic reticulum (ER) and mitochondria is critical in organelle signaling. Many of the functions regulated by ER-mitochondria signaling are disrupted in Alzheimer's disease.

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Fig. 1 The VAPB-PTPIP51 interaction is reduced in temporal cortex pyramidal neurons in Braak stage III-IV but not Braak stage VI Alzheimer's disease. Representative images of VAPB-PTPIP51 PLAs in pyramidal cells of control, Braak stage III-IV and Braak stage VI Alzheimer's disease brains.

In this study, the authors looked at the ER-mitochondria tethering proteins VAPB and PTPIP51. They found that VAPB and PTPIP51 are reduced in late-stage Alzheimer's disease in the cortex but not the cerebellum. In addition, a correlation was seen between the loss of VABP in the temporal cortex and the reductions in PTPI51, revealing a novel pathological feature in Alzheimer's disease.

  • This study used our polyclonal anti-PTPIP51/RMDN3 antibody (HPA009975, with PLA and WB) and the polyclonal anti-SigmaR1 (HPA018002, with WB) antibody.

2) Identification and characterization of novel TRPM1 autoantibodies from serum of patients with melanoma-associated retinopathy (Varin et al. 2020)

Melanoma-associated retinopathy (MAR) is a rare paraneoplastic autoimmune retinal disorder usually occurring with metastatic melanoma. MAR is characterized by the production of autoantibodies targeting retinal proteins, particularly against TRPM1. This study demonstrates that patients presenting different anti-TRPM1 autoantibodies react to the three isoforms of TRPM1 with variable binding affinity.

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Fig 2. Immunolocalization studies using the MAR sera and anti-TRPM1 antibody in COS-7 cells overexpressing the three isoforms of TRPM1.

The results suggest that a combination of different methods should be used to test for the presence of anti-TRPM1 autoantibodies in the sera of MAR patients.

  • This study used our polyclonal anti-TRPM1 (HPA014785, in ICC-IF, and WB) antibody.

3) Loss of PHF6 leads to aberrant development of human neuron-like cells (Fliedner et al. 2020)

Pathogenic variants in PHF6 cause the X-linked neurodevelopmental disorder Borjeson–Forssman–Lehmann syndrome (BFLS). In this study, the authors found evidence that de novo variants occurring in females are more severe and result in loss of PHF6, contributing to the different phenotypes in male versus female individuals. Knockout of PHF6 in neuron-like cells was examined to study related consequences of PHF6 loss.

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Fig. 3 Immunofluorescence of fibroblasts of three individuals and one control. In control, PHF6 expression could be observed in all fibroblast cells. In affected individuals, expression of PHF6 was present in 50% of cells. Cells stained our anti-PHF6 antibody.

The authors could demonstrate that intact PHF6 is necessary for proper neuron proliferation, neurite outgrowth, and migration. Impairment of these processes could contribute to the neurodevelopmental and cognitive dysfunction in BFLS.

  • This study used our polyclonal anti-PHF6 antibody (HPA001023 in ICC-IF)