By Cris dos Remedios, Deepak Chhabra
This quantity, written by means of specialists within the box, is the 1st to accommodate the connection among human affliction and the actin cytoskeleton. It offers overviews of actin and chosen actin-binding proteins, after which specializes in illnesses that contain those proteins. particular chapters care for actin, cofilin, profilin, gelsolin and thymosin ¾4. different chapters talk about the jobs of a number of actin-binding proteins in melanoma and metastasis, leukocyte issues, and middle failure, and there's a bankruptcy that describes how intracellular pathogens use the host actin cytoskeleton. This seminal quantity is meant for researchers, clinicians, physicians, and graduate scholars within the fields of biochemistry, telephone biology, microbiology, immunology, and genetics.
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This quantity, written via specialists within the box, is the 1st to accommodate the connection among human disorder and the actin cytoskeleton. It offers overviews of actin and chosen actin-binding proteins, after which specializes in illnesses that contain those proteins. particular chapters take care of actin, cofilin, profilin, gelsolin and thymosin ¾4.
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Extra resources for Actin-Binding Proteins and Disease
Kornberg, A. , Shield, L. K. and North, K. N. (2006). SEPN1: Associated with congenital fiber-type disproportion and insulin resistance. Ann. Neurol. 59, 546–552. Clarke, N. F. and North, K. N. 2003. Congenital fiber type disproportion – 30 years on. J. Neuropathol. Exp. Neurol. 62, 977–989. Conen, P. , Murphy, E. G. and Donohue, W. L. 1963. Light and electron microscopic studies of `myogranules’ in a child with hypotonia and muscle weakness. Can. Med. Assoc. J. 89, 893–896. Costa, C. , Sethi, K.
1999). Since then an increasingly large number of ACTA1 mutants causing these diseases has been identified. The count was 67 in 2003 (Sparrow et al. 2003), over 100 in 2005 (Laing and Nowak 2005) and currently stands at 116 in the report of the ENMC workshop 2006 (WallgrenPettersson and Laing 2006). , nebulin (NEB), tropomyosin (TPM2 and TPM3), troponin T (TNNT1), and cofilin (Agrawal et al. 2007). , missense mutants. Since heterozygous parents of ACTA1 null homozygous children are without clinical symptoms (Sparrow et al.
In fact, few F-actin binding proteins bind to single monomers within F-actin filaments – a mixture of wild type and mutant monomers are thus most likely to generate F-actin regions with altered affinity for specific actin-binding proteins. One might wonder why human actin mutants were not described before 1998. They have been found previously in model organisms – yeast, nematodes, and flies. However, these genomes are more readily accessible to mutagenesis and although actin mutants have been recovered in large numbers in the single yeast ACT1 actin gene (Wertman, Drubin and Botstein 1992), in Caenorhabditis elegans (Waterston, Hirsh and Lane 1984) and Drosophila melanogaster (Sparrow et al.
Actin-Binding Proteins and Disease by Cris dos Remedios, Deepak Chhabra