Fig 1: Stabilizing HSPs. (a) Under stress conditions when native proteins are destabilized and begin to unfold, stabilizing HSPs dissociate from homo- and/or heterogeneous oligomeric complexes into dimers to bind these partially misfolded proteins. Thereby, stabilizing HSPs prevent the aggregation of misfolded proteins. Figure reproduced and adapted with permission from Dorsch, L.M. et al., Pflügers Archiv–European Journal of Physiology; published by Springer Berlin Heidelberg, 2018. (b) Representative blot images for HSPB1, HSPB5, and HSPB7 expression. (c) Higher levels of HSPB1 and HSPB7 in HCMSMP (n = 38) compared to controls. Higher HSPB7 levels in HCMSMN (n = 12) compared to controls (n = 9; average is shown as dotted line). HSPB1 and HSPB5 protein levels were not different in HCMSMP (n = 14) compared to controls. There were no significant differences between HCMSMP and HCMSMN. Each dot in the scatter plots represents an individual sample. * p < 0.05 and ** p < 0.01 versus controls.
Fig 2: Schematic representation of PQC and microtubular system assessment in HCM. Our analyses show that HSPB1, HSPD1 HSPA2, a-tubulin and acetylated a-tubulin were increased in HCM, especially when a sarcomere mutation is present, while HSPB5, HSPB7, HSPA1 and degradation markers are not changed in HCM compared to controls. Levels of a-tubulin (orange balls) and acetylated a-tubulin (small yellow balls attached to a-tubulin in the lumen of polymerized microtubules (blue and orange balls)) were more increased when haploinsufficiency (HI), characterized by lower levels of cardiac myosin-binding protein-C (green lines), was the underlying pathomechanism instead of poison polypeptides (PP). =: similar to controls; ?: significantly increased compared to controls; ??: highly significantly increased compared to controls; ?: significantly decreased compared to controls.
Fig 3: Pathomechanism of HCM and key PQC players. (a) Stabilizing HSPs (HSPB1, HSPB5, HSPB7), (b) HSPs with refolding capacity (HSPD1, HSPA1 HSPA2) and (c) degradation markers (ubiquitin, p62, LC3BII) were not significantly different between HCMHI (n = 19) and HCMPP (n = 19). Each dot in the scatter plots represents an individual sample. Figure reproduced and adapted with permission from Dorsch, L.M. et al., Pflügers Archiv–European Journal of Physiology; published by Springer Berlin Heidelberg, 2018.
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