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This study showed that HNRNPA3 variants identified in Australian patients with familial amyotrophic lateral sclerosis (FALS) and associated alternate allele frequencies in cases and controls.
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Study investigated the pattern of hnRNP A1, A2/B1 and A3 immunostaining across a range of clinical, pathological and genetic forms of Frontotemporal Lobar Degeneration and Motor Neurone Disease. Data suggest there might be a derangement of movement of hnRNP A1, and other hnRNP proteins, across all pathological forms of Frontotemporal Lobar Degeneration beyond that involving just TDP-43 or FUS.
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Neurons in the hippocampus of C9orf72 patients are frequently devoid of hnRNPA3. Reduced nuclear hnRNPA3 in the hippocampus of patients with extended C9orf72 repeats correlates with increased DPR deposition.
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The results of this study suggested that mutations in hnRNPA1, A2/B1, and A3 genes are a rare finding in amyotrophic lateral sclerosis.
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characterization of hnRNP A3 in human and mouse cell lines
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Results suggest that hnRNP A3 is associated with telomere in vivo and acts as a negative regulator of telomere length maintenance.
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These biochemical properties of hnRNP A3 suggest that hnRNP A3 can participate in telomere regulation in vivo.
