A census of actin-associated proteins in humans

Figures

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  FIGURE 1. Workflow used to mine putative AAPs. The figure lists the different approaches used to identify the AAPs (A). It also lists the various downstream analyses carried out for the proteins with the tools, databases, and web servers used for the same (B).

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  FIGURE 2. Concept figure. The figure shows a schematic of the approaches to annotate AAPs from the human proteome and the number of AAPs identified from each method. Most of the proteins are present in the cytoplasm, some of the proteins associate with the membrane, and few proteins are present in organelles like the nucleus, mitochondria, ER, and the Golgi bodies.

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  FIGURE 3. Sequence and structural domains in putative AAPs. The Pfam family (A) and clan (B) distribution have been plotted as a pie chart. The top 20 domain families represent only 18% of the total Pfam families, indicating diversity. The SCOP superfamily (C), fold (D), and class distribution have been plotted. This shows the diversity of actin-binding domains in nature.

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  FIGURE 4. Functional analysis of putative AAPs. The enriched GO terms representing the biological process (A), cellular component (B), and molecular function (C) have been depicted as bar plots. The network diagrams indicate the interconnection between the GO terms in each category. The most enriched GO terms are actin filament polymerization/depolymerization (biological process), localized to the actin filament (cellular localization), and microfilament activity (molecular function).

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  FIGURE 5. Disease ontology and gene regulation details of AAPs. The KEGG pathway enrichment shows the processes related to infection, cell structures, and other disorders in the cell (A). The disease annotations have been derived from HPO (B) and OMIM (C) using the ShinyGO pipeline. These enriched annotations are for cardiomyopathy, abnormal morphology of tissues, and certain cancers. The transcription factors regulating the AAPs have been shown in (D). The AAP list shows the enrichment of transcription factors regulating ABL1 and BRCA1 genes, denoting their roles in tumor suppression.