anti-Ceroid-Lipofuscinosis, Neuronal 5 (CLN5) Antibodies

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.

list all antibodies Gene Name GeneID UniProt
CLN5 1203 O75503
CLN5 211286 Q3UMW8
CLN5 306128  
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Top anti-CLN5 Antibodies at antibodies-online.com

Showing 10 out of 71 products:

Catalog No. Reactivity Host Conjugate Application Images Quantity Delivery Price Details
Cow Rabbit Un-conjugated WB Western blot analysis of CLN5 expression in HEK293T (A), NIH3T3 (B) whole cell lysates. 200 μL 13 to 14 Days
$487.50
Details
Human Rabbit Un-conjugated ELISA, WB 100 μL Available
$363.46
Details
Human Rabbit Un-conjugated ELISA, ICC, IF, WB Western blot analysis of extracts from mouse brain, using CLN5 antibody. ABIN6274998 staining LOVO cells by IF/ICC. The sample were fixed with PFA and permeabilized in 0.1% Triton X-100,then blocked in 10% serum for 45 minutes at 25¡ãC. The primary antibody was diluted at 1/200 and incubated with the sample for 1 hour at 37¡ãC. An  Alexa Fluor 594 conjugated goat anti-rabbit IgG (H+L) antibody(Cat.# S0006), diluted at 1/600, was used as secondary antibod 100 μL 11 to 12 Days
$390.77
Details
Human Rabbit Un-conjugated WB Western blot analysis of CLN5 Antibody in T47D cell line lysates (35ug/lane) 400 μL 2 to 3 Days
$515.63
Details
Human Rabbit Un-conjugated ELISA, WB   100 μg 2 to 3 Days
$302.50
Details
Human Rabbit Un-conjugated ELISA, WB 200 μL 12 to 14 Days
$438.90
Details
Human Rabbit Un-conjugated ELISA, WB   100 μg 2 to 3 Days
$302.50
Details
Mouse Rabbit Un-conjugated WB Western blot analysis of extracts of various cell lines, using CLN5 antibody. 200 μL 12 to 14 Days
$438.90
Details
Human Rabbit PE ELISA, WB   200 μL 11 to 14 Days
$1,101.83
Details
Human Rabbit APC ELISA, WB   200 μL 11 to 14 Days
$1,101.83
Details

More Antibodies against CLN5 Interaction Partners

Human Ceroid-Lipofuscinosis, Neuronal 5 (CLN5) interaction partners

  1. This study demonstrated that Novel Mutations in CLN5 of Chinese Patients With Neuronal Ceroid Lipofuscinosis.

  2. The onset of visual deficits was much delayed. Computed tomography and MRI showed that brain structures and volumes remained stable. Because gene therapy in humans is more likely to begin after clinical diagnosis, self-complementary AAV9-CLN5 was injected into the brain ventricles of four 7-month-old affected sheep already showing early clinical signs in a second trial.

  3. We identified a missense variant in CLN5 c.A959G (p.Asn320Ser) that segregated with Alzheimer's disease. We find that this variant causes glycosylation defects in the expressed protein, which causes it to be retained in the endoplasmic reticulum with reduced delivery to the endolysosomal compartment, CLN5's normal cellular location.

  4. Genotype-phenotype correlation between CNL5 gene mutations and CNL5 disease symptoms.

  5. We conclude that, whereas sleep homeostasis is present in CLN5(-/-) sheep, underlying CLN5(-/-) disease processes prevent its full expression, even at early stages.

  6. findings support CLN5 hypomorphic mutations cause autosomal recessive cerebellar ataxia, confirming other reports showing CLN mutations are associated with adult-onset neurodegenerative disorders

  7. Two forms of CLN5, derived from the C-terminal proteolytic processing, are present in most cells and tissues.

  8. There are functional differences in various N-glycosylation sites of CLN5 which affect folding, trafficking, and lysosomal function of CLN5.

  9. a role for CLN5 in controlling the itinerary of the lysosomal sorting receptors by regulating retromer recruitment at the endosome

  10. This study highlights a close interaction between CLN5/CLN8 proteins, and their role in sphingolipid metabolism. Our findings suggest that CLN5p/CLN8p most likely are positive modulators of CerS1 and/or CerS2.

  11. analysis of mutations in neuronal ceroid lipofuscinosis protein CLN5

  12. CLN5 mutations are 1) more common in patients with neuronal ceroid lipofuscinosis (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

  13. Study found that CLN5 interacts with several other NCL proteins namely, CLN1/PPT1, CLN2/TPP1, CLN3, CLN6 and CLN8.

  14. biosynthesis and intracellular localization of this protein

  15. juvenile and variant late infantile neuronal ceroid lipofuscinoses have mutated CLN genes encoding lysosomal proteins (review)

  16. Data show that three neuronal ceroid lipofuscinoses disease forms with similar tissue pathology are connected at the molecular level: CLN5 polypeptides directly interact with the CLN2 and CLN3 proteins

  17. A novel missense mutation in CLN5 was found in a Colombian family with juvenile-onset neuronal ceroid lipofuscinosis: c. 1627G>A causing Arg112His.

  18. The CLN5/mRNA expression level reduced to 45% supports the existence of one mRNA non-producing allele, further noticeable at the protein level.

  19. Reports two sibs harbouring a novel mutation (p.Tyr258Asp) in the CLN5 gene and displaying behaviour disturbances and mental deterioration, rather than epilepsy, as the dominant disease manifestation at onset.

  20. In cultures of brain microvascular endothelial cells, VEGF-A specifically down-regulated CLN-5 and OCLN protein and mRNA

Mouse (Murine) Ceroid-Lipofuscinosis, Neuronal 5 (CLN5) interaction partners

  1. Quantification revealed that the amounts of 12 different soluble lysosomal proteins were significantly reduced in Cln7 ko MEFs compared with wild-type controls. One of the most significantly depleted lysosomal proteins was Cln5 protein that underlies another distinct neuronal ceroid lipofuscinosis disorder

  2. neurogenesis is increased in Cln5-deficient mice, which model the childhood neurodegenerative disorder caused by loss of Cln5.

  3. Rssults suggested that CLN2, CLN3 and CLN5 genes may play an important role in early embryonal neurogenesis.

  4. The simultaneous loss of both Cln1 and Cln5 genes might enhance the typical pathological phenotypes of these mice by disrupting or downregulating shared or convergent pathogenic pathways.

  5. 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.

  6. Study found that CLN5 interacts with several other NCL proteins namely, CLN1/PPT1, CLN2/TPP1, CLN3, CLN6 and CLN8.

  7. 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.

  8. because the role of the functionally uncharacterized Cln5 protein remains unclear these studies may offer clues to the unraveling of its possible function(s)

  9. In mouse cerebral cortex, microinjection of VEGF-A disrupted CLN-5 and OCLN and induced loss of barrier function

  10. 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.

Cow (Bovine) Ceroid-Lipofuscinosis, Neuronal 5 (CLN5) interaction partners

  1. The candidate genes for bovine Neuronal Ceroid Lipofuscinosis,CLN3 , CLN5 and CLN6, have been mapped to facilitate linkage analysis in cattle and sheep.

CLN5 Antigen Profile

Protein Summary

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.

Gene names and symbols associated with CLN5

  • CLN5, intracellular trafficking protein (CLN5) antibody
  • ceroid-lipofuscinosis, neuronal 5 (Cln5) antibody
  • CLN5, intracellular trafficking protein (Cln5) antibody
  • A730075N08Rik antibody
  • NCL antibody

Protein level used designations for CLN5

ceroid-lipofuscinosis neuronal protein 5 , ceroid-lipofuscinosis neuronal protein 5 homolog , ceroid-lipofuscinosis neuronal 5

GENE ID SPECIES
1203 Homo sapiens
211286 Mus musculus
529186 Bos taurus
485498 Canis lupus familiaris
100034668 Ovis aries
306128 Rattus norvegicus
100152208 Sus scrofa
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