HPA023269
Anti-NIPA1 antibody produced in rabbit
Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Synonym(s):
Anti-Non-imprinted in Prader-Willi/Angelman syndrome region protein 1
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
product line
Prestige Antibodies® Powered by Atlas Antibodies
form
buffered aqueous glycerol solution
species reactivity
human
technique(s)
immunohistochemistry: 1:20- 1:50
immunogen sequence
HGPTNIMVYISICSLLGSFTVPSTKGIGLAAQDILHNNPSSQRA
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... NIPA1(123606)
Related Categories
General description
The gene NIPA1 (non-imprinted in Prader-Willi/Angelman syndrome 1) is mapped to human chromosome 15q11. The protein is predicted to have nine transmembrane segments. It is widely expressed with strong expression in the brain.
Immunogen
Non-imprinted in Prader-Willi/Angelman syndrome region protein 1 recombinant protein epitope signature tag (PrEST)
Application
All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.
The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.
The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.
Biochem/physiol Actions
NIPA1 (non-imprinted in Prader-Willi/Angelman syndrome 1) might be involved in intracellular magnesium transport. In Drosophila, NIPA1 homolog spichthyin participates in bone morphogenic protein (BMP)-linked signaling pathways and is needed for synaptic development and axonal maintenance. Mutations in NIPA1 are associated with hereditary spastic paraplegia. NIPA1 polyalanine repeat expansions result in amyotrophic lateral sclerosis (ALS) pathogenesis.
Features and Benefits
Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.
Every Prestige Antibody is tested in the following ways:
Every Prestige Antibody is tested in the following ways:
- IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
- Protein array of 364 human recombinant protein fragments.
Physical form
Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide
Other Notes
Corresponding Antigen APREST70271
Legal Information
Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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Pure hereditary spastic paraplegia due to a de novo mutation in the NIPA1 gene.
D Arkadir et al.
European journal of neurology, 21(1), e2-e2 (2014-08-19)
Hylke M Blauw et al.
Human molecular genetics, 21(11), 2497-2502 (2012-03-02)
Mutations in NIPA1 cause Hereditary Spastic Paraplegia type 6, a neurodegenerative disease characterized by an (upper) motor neuron phenotype. Deletions of NIPA1 have been associated with a higher susceptibility to amyotrophic lateral sclerosis (ALS). The exact role of genetic variation
Hylke M Blauw et al.
Human molecular genetics, 19(20), 4091-4099 (2010-08-06)
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease selectively affecting motor neurons in the brain and spinal cord. Recent genome-wide association studies (GWASs) have identified several common variants which increase disease susceptibility. In contrast, rare copy-number variants (CNVs), which
Jiali Zhao et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 28(51), 13938-13951 (2008-12-19)
We studied the consequences of expression of wild-type (WT) human NIPA1 and two mutant forms of NIPA1 with known HSP-associated mutations (T45R and G106R) on cultured rat cortical neurons and using equivalent substitutions in the Caenorhabditis elegans NIPA1 homolog CeNIPA.
Shirley Rainier et al.
American journal of human genetics, 73(4), 967-971 (2003-09-26)
The hereditary spastic paraplegias (HSPs) are genetically heterogeneous disorders characterized by progressive lower-extremity weakness and spasticity. The molecular pathogenesis is poorly understood. We report discovery of a dominant negative mutation in the NIPA1 gene in a kindred with autosomal dominant
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