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Home  >  ELISA Kit  >  Human MFSD8 ELISA Kit
MFSD8 (GeneName), Major facilitator superfamily domain-containing protein 8 (ProteinName), MFSD8_HUMAN.
Product Name:

Human MFSD8/ Major facilitator superfamily domain-containing protein 8 ELISA Kit

Cat.#:
-
Brand:
EIAab®
Regulatory Status:
Alternative:

Ceroid-lipofuscinosis neuronal protein 7, CLN7

Detection Method:
ELISA
Specificity:
Natural and recombinant human Major facilitator superfamily domain-containing protein 8
Sample Type:
Serum, plasma, tissue homogenates, cell culture supernates and other biological fluids
Sample Data:
Research Area:
-
Human MFSD8 ELISA Kit
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Human MFSD8 ELISA Kit
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Product Datasheets


General Annotation


Sub Unit:
N/A


Function:
May be a carrier that transport small solutes by using chemiosmotic ion gradients.


Subcellular Location:
Lysosome membrane Multi-pass membrane protein Sorting to lysosomes involves tyrosine- and/or dileucine-based motifs.


This product has not yet been referenced specifically in any publications.

[1].
"The novel neuronal ceroid lipofuscinosis gene MFSD8 encodes a putative lysosomal transporter."

[2].
"Mutations in MFSD8, encoding a lysosomal membrane protein, are associated with nonsyndromic autosomal recessive macular dystrophy."

[3].
"A novel mutation in the MFSD8 gene in late infantile neuronal ceroid lipofuscinosis."

[4].
"Mutations in MFSD8/CLN7 are a frequent cause of variant-late infantile neuronal ceroid lipofuscinosis."

[5].
"Mutations in CLN7/MFSD8 are a common cause of variant late-infantile neuronal ceroid lipofuscinosis."

[6].
"Neuronal ceroid lipofuscinosis caused by MFSD8 mutations: a common theme emerging."

[7].
"Integral and associated lysosomal membrane proteins."

[8].
"Architecture of the human interactome defines protein communities and disease networks."

[9].
"Specific Alleles of CLN7/MFSD8, a Protein That Localizes to Photoreceptor Synaptic Terminals, Cause a Spectrum of Nonsyndromic Retinal Dystrophy."

[10].
"The BioPlex Network: A Systematic Exploration of the Human Interactome."
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