MABN473
Anti-TMEM106B Antibody, clone TME-N 6F2
clone TME-N 6F2, from rat
Synonym(s):
Transmembrane protein 106B, TMEM106B
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rat
Quality Level
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
TME-N 6F2, monoclonal
species reactivity
rat, human
technique(s)
immunofluorescence: suitable
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... TMEM106B(54664)
General description
Transmembrane protein 106B (TMEM106B) is a single-pass type II membrane protein present in endosomal and lysosomal membranes, and is highly expressed in the frontal cortex. Increased TMEM106B expression in the brain may be linked to mechanisms of disease in frontotemporal lobar degeneration with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP). Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia.
Specificity
This antibody recognizes the N-terminus of TMEM106B.
Immunogen
Epitope: N-terminus
Recombinant protein corresponding to the N-terminus of human TMEM106B.
Application
Anti-TMEM106B, clone TME-N 6F2 detects levels of TMEM106B proteins & has been published & validated for use in WB & IF.
Immunofluorescence Analysis: A 1:50 dilution from a representative lot detected TMEM106B in rat cerebellum tissue.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Neurodegenerative Diseases
Quality
Evaluated by Western Blot in human cortex tissue lysate.
Western Blot Analysis: 1 µg/mL of this antibody detected TMEM106B in 10 µg of human cortex tissue lysate.
Western Blot Analysis: 1 µg/mL of this antibody detected TMEM106B in 10 µg of human cortex tissue lysate.
Target description
~30 kDa observed (At higher antibody concentrations, this protein may be observed at ~45 kDa). This protein may be observed at ~50 kDa due to glycosylation (Lang, C. M., et al. (2012). J Biol Chem. 287(23):19355-19365.).
Physical form
Format: Purified
Protein G Purified
Purified rat monoclonal IgG2c in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Storage and Stability
Stable for 1 year at 2-8°C from date of receipt.
Analysis Note
Control
Human cortex tissue lysate
Human cortex tissue lysate
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
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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Storage Class
12 - Non Combustible Liquids
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Christina M Lang et al.
The Journal of biological chemistry, 287(23), 19355-19365 (2012-04-19)
TMEM106B was identified as a major risk factor in a genome-wide association study for frontotemporal lobar degeneration (FTLD) with TAR DNA-binding protein (TDP)-43 pathology. The most significant association of TMEM106B single nucleotide polymorphisms with risk of FTLD-TDP was observed in
Benjamin M Schwenk et al.
The EMBO journal, 33(5), 450-467 (2013-12-21)
TMEM106B is a major risk factor for frontotemporal lobar degeneration with TDP-43 pathology. TMEM106B localizes to lysosomes, but its function remains unclear. We show that TMEM106B knockdown in primary neurons affects lysosomal trafficking and blunts dendritic arborization. We identify microtubule-associated
Common pathobiochemical hallmarks of progranulin-associated frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis.
Gotzl, JK; Mori, K; Damme, M; Fellerer, K; Tahirovic, S; Kleinberger, G; Janssens et al.
Acta neuropathologica null
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