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Actinin, alpha 4

alpha-actinin-4, ACTN4, actinin-4
Alpha actinins belong to the spectrin gene superfamily which represents a diverse group of cytoskeletal proteins, including the alpha and beta spectrins and dystrophins. Alpha actinin is an actin-binding protein with multiple roles in different cell types. In nonmuscle cells, the cytoskeletal isoform is found along microfilament bundles and adherens-type junctions, where it is involved in binding actin to the membrane. In contrast, skeletal, cardiac, and smooth muscle isoforms are localized to the Z-disc and analogous dense bodies, where they help anchor the myofibrillar actin filaments. This gene encodes a nonmuscle, alpha actinin isoform which is concentrated in the cytoplasm, and thought to be involved in metastatic processes. Mutations in this gene have been associated with focal and segmental glomerulosclerosis. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: alpha-Actinin, Actin, Nephrin, CAN, HAD
Papers on alpha-actinin-4
Three-layered proteomic characterization of a novel ACTN4 mutation unravels its pathogenic potential in FSGS.
Beck et al., Köln, Germany. In Hum Mol Genet, Feb 2016
Mutations in the ACTN4 gene, encoding the actin-binding protein alpha-actinin-4, are a rare cause of autosomal dominant familial focal segmental glomerulosclerosis (FSGS).
A complex of Rab13 with MICAL-L2 and α-actinin-4 is essential for insulin-dependent GLUT4 exocytosis.
Klip et al., Toronto, Canada. In Mol Biol Cell, Feb 2016
Insulin further increased binding of MICAL-L2 to α-actinin-4 (ACTN4), a protein involved in GLUT4 translocation.
Effects of stromal interaction molecule 1 or Orai1 over-expression on the associated proteins and permeability of podocytes.
Huang et al., Nanjing, China. In Nephrology (carlton), Jan 2016
STIM1/Orai1 over-expression significantly decreased the expression of podocin and CD2-associated protein (CD2AP), whereas it increased the expression of α-actinin-4.
Traumatically injured astrocytes release a proteomic signature modulated by STAT3-dependent cell survival.
Wanner et al., Los Angeles, United States. In Glia, Jan 2016
STAT3-CKO astrocytes had reduced basal expression of GFAP, lactate dehydrogenase B (LDHB), aldolase C (ALDOC), and astrocytic phosphoprotein 15 (PEA15), and elevated levels of tropomyosin (TPM4) and α actinin 4 (ACTN4).
Synaptopodin couples epithelial contractility to α-actinin-4-dependent junction maturation.
Tang et al., Champaign, United States. In J Cell Biol, Nov 2015
We found that mechanical force induces α-actinin-4 and actin accumulation at the cell junction in a time- and tension-dependent manner during junction development.
NHERF1 regulates actin cytoskeleton organization through modulation of α-actinin-4 stability.
He et al., Beijing, China. In Faseb J, Nov 2015
α-Actinin-4, an actin cross-linking protein, was identified.
Focal segmental glomerulosclerosis: molecular genetics and targeted therapies.
Liapis et al., Saint Louis, United States. In Bmc Nephrol, 2014
Recent advances show that human focal segmental glomerulosclerosis (FSGS) is a primary podocytopathy caused by podocyte-specific gene mutations including NPHS1, NPHS2, WT-1, LAMB2, CD2AP, TRPC6, ACTN4 and INF2.
PDLIM1 inhibits NF-κB-mediated inflammatory signaling by sequestering the p65 subunit of NF-κB in the cytoplasm.
Tanaka et al., Yokohama, Japan. In Sci Rep, 2014
PDLIM1 sequestered p65 subunit of NF-κB in the cytoplasm and suppressed its nuclear translocation in an IκBα-independent, but α-actinin-4-dependent manner.
New developments in steroid-resistant nephrotic syndrome.
Saleem, Bristol, United Kingdom. In Pediatr Nephrol, 2013
Key genes that have been identified from the study of inherited nephrotic syndromes include those encoding nephrin, podocin, TRPC6 (transient receptor potential canonical channel-6) and α-actinin-4, and more remain to be found.
Alpha-actinin 4 and tumorigenesis of breast cancer.
Kao et al., Cleveland, United States. In Vitam Horm, 2012
Notably, unlike other ACTNs, alpha-actinin 4 (ACTN4) displays unique characteristics in signaling transduction, nuclear translocation, and gene expression regulation.
MDM2 binding protein, a novel metastasis suppressor.
Agarwal et al., Kansas City, United States. In Cancer Metastasis Rev, 2012
Furthermore, overexpression of MTBP suppresses cell migration and filopodia formation, in part, by inhibiting function of an actin crosslinking protein α-actinin-4.
Involvements of the ABC protein ABCF2 and α-actinin-4 in regulation of cell volume and anion channels in human epithelial cells.
Okada et al., Suzuka, Japan. In J Cell Physiol, 2012
The ACTN4-ABCF2 interaction was markedly enhanced by hypotonic stimulation.
ACTN4 gene amplification and actinin-4 protein overexpression drive tumour development and histological progression in a high-grade subset of ovarian clear-cell adenocarcinomas.
Matsubara et al., Saitama, Japan. In Histopathology, 2012
In 12 of 23 ACTN4-amplified ovarian clear-cell adenocarcinomas, the better differentiated carcinoma components exhibited fewer alterations than those with poorly differentiated histology.
Calcium sensitivity of α-actinin is required for equatorial actin assembly during cytokinesis.
Murata-Hori et al., Singapore, Singapore. In Cell Cycle, 2012
The calcium sensitivity of alpha-actinin is required for its equatorial accumulation that is crucial for the initial equatorial actin assembly but is dispensable for cytokinesis.
Familial focal segmental glomerulosclerosis (FSGS)-linked α-actinin 4 (ACTN4) protein mutants lose ability to activate transcription by nuclear hormone receptors.
Kao et al., Cleveland, United States. In J Biol Chem, 2012
the first link between focal segmental glomerulosclerosis-linked ACTN4 mutants and transcriptional activation by nuclear receptor such as RARalpha and peroxisome proliferator-activated receptor gamma.
[Novel splicing isoform of actin-binding protein alpha-actinin 4 in epidermoid carcinoma cells A431].
Tentler et al., In Tsitologiia, 2011
A novel ACTN4 isoform was found in human epidermoid carcinoma cells. Analysis of ACTN4 mRNA showed the presence of a splice variant that lacked the exons 2-8.
Alpha-actinin: a multidisciplinary protein with important role in B-cell driven autoimmunity.
Dalekos et al., Lárisa, Greece. In Autoimmun Rev, 2011
Four isoforms of human α-actinin have already been identified namely, the "muscles" α-actinin-2 and α-actinin-3 and the "non-muscles" α-actinin-1 and α-actinin-4.
Pathogenesis of nonimmune glomerulopathies.
Shaw et al., Saint Louis, United States. In Annu Rev Pathol, 2005
In addition, we review our current understanding of the slit diaphragm (a specialized cell junction found in the kidney), slit diaphragm-associated proteins (including nephrin, podocin, alpha-actinin-4, CD2-associated protein, and transient receptor potential channel 6), and the role of these proteins in glomerular disease.
Rab5 is a signalling GTPase involved in actin remodelling by receptor tyrosine kinases.
Di Fiore et al., Milano, Italy. In Nature, 2004
Finally, RN-tre interacts with both F-actin and actinin-4, an F-actin bundling protein.
Mutations in ACTN4, encoding alpha-actinin-4, cause familial focal segmental glomerulosclerosis.
Pollak et al., Boston, United States. In Nat Genet, 2000
Here we present evidence implicating mutations in the gene encoding alpha-actinin-4 (ACTN4; ref. 2), an actin-filament crosslinking protein, as the cause of disease in three families with an autosomal dominant form of FSGS.
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