• In this paper, we show with direct mechanical single-molecule measurements that an array of titin/α-actinin bonds composes a dynamic network that can provide stable anchoring, maintaining the integrity of the muscle Z-disk even under load. (pnas.org)
  • One of the main candidates for anchoring titin in the Z-disk is the actin cross-linker α-actinin. (pnas.org)
  • The calmodulin-like domain of α-actinin binds to the Z-repeats of titin. (pnas.org)
  • Our results suggest a model where multiple α-actinin/Z-repeat interactions cooperate to ensure long-term stable titin anchoring while allowing the individual components to exchange dynamically. (pnas.org)
  • B ) Arrangement of actin, titin, telethonin, and α-actinin within the Z-disk. (pnas.org)
  • Alpha-actinin interactions with syndecan-4 are integral to fibroblast-matrix adhesion and regulate cytoskeletal architecture. (nih.gov)
  • Title: Arf6 guanine-nucleotide exchange factor, cytohesin-2, interacts with actinin-1 to regulate neurite extension. (nih.gov)
  • More broadly though, this structure presents a picture of the intimate interactions between the subunits in the actinin dimer, providing a framework to better understand the molecular details of actin cross-linking and its regulation in all actinins and perhaps in spectrins too. (springer.com)
  • Solid phase binding assays indicated that alpha-actinin bound specifically and directly to the beta 1 peptide with relatively high affinity. (pubmedcentralcanada.ca)
  • Using purified heterodimeric chicken smooth muscle integrin (a beta 1 integrin) or the platelet integrin glycoprotein IIb/IIIa complex (a beta 3 integrin), binding of alpha-actinin was also observed in similar solid phase assays, albeit with a lower affinity than was seen using the beta 1 peptide. (pubmedcentralcanada.ca)
  • Defects in the gene encoding α-actinin-4 are the cause of focal segmental glomerulosclerosis 1 (FSGS1), a common renal lesion characterized by decreasing kidney function and, ultimately, renal failure. (acris-antibodies.com)
  • Considering the fact that the active construct is "always on" because it requires nonphysiological, high Ca2+ concentrations for inactivation, it is interesting to note that an unregulated alpha-actinin was able to rescue the mutant phenotype. (rupress.org)
  • These results provide further support that alpha-actinin-3 deficient individuals may experience faster decline in muscle function with increasing age. (garvan.org.au)