Render Target: STATIC
Render Timestamp: 2025-03-14T11:00:23.338Z
Commit: a619ae74f66dae0f27639e88da12bcf600e46428
XML generation date: 2025-03-07 13:14:53.068
Product last modified at: 2025-03-03T15:15:08.842Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

SMCR8 Antibody #35396

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 140-150
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    SMCR8 Antibody recognizes endogenous levels of total SMCR8 protein. A band of unknown origin is detected at around 70 kDa.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala540 of human SMCR8 protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    SMCR8 (Smith-Magenis chromosome region 8) was characterized as a member of the DENN (differentially expressed in normal and neoplastic cells) domain family that typically function in intracellular membrane trafficking as guanine exchange factors for Rab GTPases (1). Deletion of the SMCR8 gene was found in patients having Smith-Magenis syndrome, a rare developmental disorder (2,3). SMCR8 interacts with another DENN protein C9orf72, and the WD repeat containing protein WDR41, that function as a guanine exchange factor for Rab8a and Rab39b and regulate autophagy (4). Interestingly, C9orf72 is also associated with neurodegenerative diseases including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) (5,6). C9orf72 and SMCR8 were found to have multifaceted roles in autophagy and lysosomal signaling (reviewed 7). SMCR8 can be phosphorylated by kinases with roles in autophagy including TBK1 and ULK1 (4). Indeed, the complex containing C9orf72, SMCR8, and WDR41 associates with the ULK1 complex essential for initiation of autophagy (8). Furthermore, SMCR8 was found in an RNAi screen as a regulator of ULK1 activity and both initiation and maturation of autophagosomes (9). Knockdown of SMCR8 in vivo has led to inflammatory and autoimmune phenotypes as well as inhibition of autophagy, elevated activity of mTORC1 and Akt, and decreased lysosomal biogenesis (10-13).
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