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CLN5 is one of eight which have been associated with neuronal ceroid lipofuscinoses (NCL). Additionally we are shipping CLN5 Proteins (6) and many more products for this protein.
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We conclude that, whereas sleep homeostasis is present in CLN5(-/-) sheep, underlying CLN5(-/-) disease processes prevent its full expression, even at early stages.
findings support CLN5 hypomorphic mutations cause autosomal recessive cerebellar ataxia, confirming other reports showing CLN (show CLGN Antibodies) mutations are associated with adult-onset neurodegenerative disorders
Two forms of CLN5, derived from the C-terminal proteolytic processing, are present in most cells and tissues.
There are functional differences in various N-glycosylation sites of CLN5 which affect folding, trafficking, and lysosomal function of CLN5.
a role for CLN5 in controlling the itinerary of the lysosomal sorting receptors by regulating retromer recruitment at the endosome
This study highlights a close interaction between CLN5/CLN8 (show CLN8 Antibodies) proteins, and their role in sphingolipid metabolism. Our findings suggest that CLN5p/CLN8p most likely are positive modulators of CerS1 (show CERS1 Antibodies) and/or CerS2 (show CERS2 Antibodies).
analysis of mutations in neuronal ceroid lipofuscinosis (show CLN6 Antibodies) protein CLN5
CLN5 mutations are 1 (show VPS52 Antibodies)) more common in patients with neuronal ceroid lipofuscinosis (show CLN6 Antibodies) (NCL) than previously reported, 2) found in patients of broad ethnic diversity, and 3) can be identified in patients with disease onset in adult and juvenile epochs
Study found that CLN5 interacts with several other NCL proteins namely, CLN1/PPT1 (show PPT1 Antibodies), CLN2/TPP1 (show TPP1 Antibodies), CLN3 (show CLN3 Antibodies), CLN6 (show CLN6 Antibodies) and CLN8 (show CLN8 Antibodies).
juvenile and variant late infantile neuronal ceroid lipofuscinoses have mutated CLN (show CLGN Antibodies) genes encoding lysosomal proteins (review)
neurogenesis is increased in Cln5-deficient mice, which model the childhood neurodegenerative disorder caused by loss of Cln5.
Rssults suggested that CLN2 (show TPP1 Antibodies), CLN3 (show CLN3 Antibodies) and CLN5 genes may play an important role in early embryonal neurogenesis.
The simultaneous loss of both Cln1 (show PPT1 Antibodies) and Cln5 genes might enhance the typical pathological phenotypes of these mice by disrupting or downregulating shared or convergent pathogenic pathways.
In Cln5-deficient mice, early and significant microglial activation is documented that is already evident at 3 months of age; it increases gradually with age and differs between neurons and glia, with the highest expression in microglia.
Study found that CLN5 interacts with several other NCL (show NCL Antibodies) proteins namely, CLN1/PPT1 (show PPT1 Antibodies), CLN2/TPP1 (show TPP1 Antibodies), CLN3 (show CLN3 Antibodies), CLN6 (show CLN6 Antibodies) and CLN8 (show CLN8 Antibodies).
Mouse Cln5 is a soluble lysosomal glycoprotein expressed throughout embryonic brain, increasing during development; prominent expression is observed in cerebellar Purkinje cells, cerebral neurons, hippocampal pyramidal cells, and hippocampal interneurons.
because the role of the functionally uncharacterized Cln5 protein remains unclear these studies may offer clues to the unraveling of its possible function(s)
In mouse cerebral cortex, microinjection of VEGF-A (show VEGFA Antibodies) disrupted CLN-5 and OCLN (show OCLN Antibodies) and induced loss of barrier function
These data provide unexpected evidence for a distinctive sequence of neuron loss in the thalamocortical system of Cln5-/- mice, diametrically opposed to that seen in other forms of NCL (show NCL Antibodies).
The candidate genes for bovine Neuronal Ceroid Lipofuscinosis (show CLN6 Antibodies),CLN3 (show CLN3 Antibodies) , CLN5 and CLN6 (show CLN6 Antibodies), have been mapped to facilitate linkage analysis in cattle and sheep.
This gene is one of eight which have been associated with neuronal ceroid lipofuscinoses (NCL). Also referred to as Batten disease, NCL comprises a class of autosomal recessive, neurodegenerative disorders affecting children. The genes responsible likely encode proteins involved in the degradation of post-translationally modified proteins in lysosomes. The primary defect in NCL disorders is thought to be associated with lysosomal storage function.
ceroid-lipofuscinosis neuronal protein 5
, ceroid-lipofuscinosis neuronal protein 5 homolog
, ceroid-lipofuscinosis neuronal 5