|Positive WB detected in||U2OS cells, HeLa cells, K-562 cells, LNCaP cells, A549 cells, Jurkat cells|
|Positive IP detected in||HeLa cells|
|Western Blot (WB)||WB : 1:5000-1:50000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:500-1:1000 for WB|
|Sample-dependent, check data in validation data gallery|
60333-1-Ig targets TMEM106B in WB, IP, IHC, ELISA applications and shows reactivity with human samples.
|Host / Isotype||Mouse / IgG1|
|Immunogen||TMEM106B fusion protein Ag21448|
|Full Name||transmembrane protein 106B|
|Calculated molecular weight||31 kDa|
|Observed molecular weight||~40 kDa|
|GenBank accession number||BC033901|
|Gene ID (NCBI)||54664|
|Purification Method||Protein G purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage. 20ul sizes contain 0.1% BSA.|
TMEM106B is a genetic risk factor for frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). Amyotrophic lateral sclerosis (ALS), like FTLD-TDP, is characterized by pathological TDP-43 inclusions. TMEM106B expression in the brain may be linked to mechanisms of disease in FTLD-TDP and risk alleles confer genetic susceptibility by increasing gene expression.
Homotypic fibrillization of TMEM106B across diverse neurodegenerative diseases.
C-terminal TMEM106B fragments in human brain correlate with disease-associated TMEM106B haplotypes
Accumulation of TMEM106B C-terminal fragments in neurodegenerative disease and aging
Front Cell Neurosci
Loss of TMEM106B exacerbates C9ALS/FTD DPR pathology by disrupting autophagosome maturation