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Plastins are a family of actin-binding proteins that are conserved throughout eukaryote evolution and expressed in most tissues of higher eukaryotes. Additionally we are shipping Plastin 3 Antibodies (61) and many more products for this protein.
Showing 10 out of 14 products:
PLS3 mutation plays a role in low turnover osteoporosis pathophysiology.
In this study, the authors found that the actin filament bundling abilities of PLS1 (show PLS1 Proteins) and PLS2 (show LCP1 Proteins) were similarly sensitive to Ca(2 (show CA2 Proteins)+) (pCa50 ~6.4), whereas PLS3 was less sensitive (pCa50 ~5.9).
Patients with PLS3 mutation-related osteoporosis respond to teriparatide treatment.
We show that genes of the classical apoptosis pathway are involved in the smn-1 (show SMN1 Proteins)-mediated neuronal death, and that this phenotype can be rescued by the expression of human SMN1 (show SMN1 Proteins), indicating a functional conservation between the two orthologs. Finally, we determined that Plastin3/plst-1 genetically interacts with smn-1 (show SMN1 Proteins) to prevent degeneration, and that treatment with valproic acid is able to rescue the degenerative phenotype
PLS3 expression does not always modify SMA (show SMN1 Proteins) phenotype
findings emphasize the power of genetic modifiers, PLS3 and CORO1C (show CORO1C Proteins), to unravel the cellular pathomechanisms underlying spinal muscular atrophy (SMA (show SMN1 Proteins))--and the power of combinatorial therapy based on splice correction of SMN2 (show SMN1 Proteins) and endocytosis improvement to efficiently treat SMA (show SMN1 Proteins)
PLS3 is a genuine spinal muscular atrophy protective modifier in SMN1 (show SMN1 Proteins)-deleted individuals
Measurements of SMN (show STMN1 Proteins) and PLS3 transcript and protein levels in induced pluripotent stem cell-derived motor neurons show limited value as Spinal muscular atrophy biomarkers.
High levels of recombinant hPLS3 mRNA were expressed in motor neurons of SMA (show SMN1 Proteins) mice and an increased level of PLS3 protein in total spinal cord, yet neither survival nor the fundamental electrophysiological aspects of the neuromuscular junction improved.
results confirm the role of PLS3 mutations in early onset osteoporosis. The mechanism whereby PLS3 affects bone health is unclear, but it may be linked to osteocyte dendrite function and skeletal mechanosensing
Depletion of Pls3 transcripts in mouse embryos caused basement membrane and polarity defects in the epidermis which were secondary to the disruption of the basement membrane but had little effect on cell adhesion and differentiation.
Plastins are a family of actin-binding proteins that are conserved throughout eukaryote evolution and expressed in most tissues of higher eukaryotes. In humans, two ubiquitous plastin isoforms (L and T) have been identified. Plastin 1 (otherwise known as Fimbrin) is a third distinct plastin isoform which is specifically expressed at high levels in the small intestine. The L isoform is expressed only in hemopoietic cell lineages, while the T isoform has been found in all other normal cells of solid tissues that have replicative potential (fibroblasts, endothelial cells, epithelial cells, melanocytes, etc.). The C-terminal 570 amino acids of the T-plastin and L-plastin proteins are 83% identical. It contains a potential calcium-binding site near the N terminus. Alternate splicing results in multiple transcript variants.
, plastin 3 (T isoform)
, T fimbrin
, T plastin
, plastin 3 (T-isoform)
, plastin 3, T