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I0282

Sigma-Aldrich

Anti-α-Internexin antibody, Mouse monoclonal

clone 2E3, purified from hybridoma cell culture

Synonym(s):

Anti-66 kDa Neurofilament Subunit, Anti-INA, Anti-NF-66

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified from hybridoma cell culture

antibody product type

primary antibodies

clone

2E3, monoclonal

form

buffered aqueous solution

mol wt

antigen ~66 kDa by SDS-PAGE

species reactivity

feline, rat, bovine, human, pig

concentration

~2 mg/mL

technique(s)

immunocytochemistry: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
microarray: suitable
western blot: 0.5 μg/mL using rat brain cytosolic extract

isotype

IgG1

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... INA(9118)
rat ... Ina(24503)

General description

Monoclonal Anti-α -Internexin (mouse IgG1 isotype) is derived from the 2E3 hybridoma produced by the fusion of mouse myeloma cells and splenocytes from mice immunized with the full-length recombinant rat α -internexin.
The gene INA (α-Internexin) encodes a neuronal intermediate filament (IF) protein that is a type IV IF. The gene is mapped to human chromosome 10. The encoded protein has a molar mass of 55.4kDa and spans a length of 499 amino acids. It is expressed in the neurons along with the NF (neurofilament) triplet proteins, NF-L (light), NF-M (medium), NF-H (heavy).

Immunogen

full-length recombinant rat α-internexin.

Application

Anti-α-Internexin antibody, Mouse monoclonal has been used in:
  • enzyme linked immunosorbent assay (ELISA)
  • immunoblotting
  • immunohistochemistry
  • immunocytochemistry

Biochem/physiol Actions

The expression of α-Internexin precedes the expression of NF triplet proteins during the differentiation of neurons. Its expression is relatively low when compared to the the NF proteins in the adult brain. It co-assembles with the NF triplet proteins. Overexpression of α-internexin in transgenic mouse model has been found to cause abnormal neurofilamentous accumulations and motor coordination deficits. It has been found to be present in cytoplasmic inclusions linking it to NIFID (neuronal intermediate filament inclusion disease) and other neurological diseases with pathological accumulations of IFs (intermediate filaments). α-Internexin may be useful as a biomarker for pancreatic neuroendocrine tumor aggressiveness and prognosis.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, and 15 mM sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Julien, J.P., and et al.
Prog. Nucleic Acids Res. Mol. Biol., 61, 1-1 (1998)
Nestin in immature embryonic neurons affects axon growth cone morphology and Semaphorin3a sensitivity
Bott CJ, et al.
Molecular Biology of the Cell, 30(10), 1214-1229 (2019)
Jenafer Evans et al.
Journal of neurophysiology, 87(2), 1076-1085 (2002-02-05)
Embryonic or neonatal rat neurons retain plasticity and are readily grown in tissue culture, but neurons of the adult brain were thought to be terminally differentiated and therefore difficult to culture. Recent studies, however, suggest that it may be possible
Bei Liu et al.
The Journal of clinical endocrinology and metabolism, 99(5), E786-E795 (2014-02-04)
We aimed to test whether α-internexin could be a molecular biomarker of tumor aggressiveness and prognosis in pancreatic neuroendocrine tumors (PNETs). Using immunohistochemical staining and Western blot, we detected the expression of α-internexin in 350 tumors from 343 patients, of
Nigel J Cairns et al.
The American journal of pathology, 164(6), 2153-2161 (2004-05-27)
Neuronal intermediate filament (IF) inclusion disease (NIFID) is a novel neurological disease of early onset with a variable clinical phenotype including frontotemporal dementia, pyramidal, and extrapyramidal signs. Pathologically, in affected areas, there is neuronal loss, astrocytosis, and neuronal intracytoplasmic aggregates

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