Render Target: SSR
Render Timestamp: 2024-12-19T21:46:19.162Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:59:51.840
Product last modified at: 2024-09-30T08:01:54.752Z
Cell Signaling Technology Logo
1% for the planet logo
PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

TMEM41B (F6F4Z) Rabbit mAb #30518

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 22
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    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, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    TMEM41B (F6F4Z) Rabbit mAb recognizes endogenous levels of total TMEM41B protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human TMEM41B protein.

    Background

    TMEM41B (also known as Stasimon) was discovered as a target of splicing dysfunction induced by loss of spinal motor neuron (SMN) protein, a feature of spinal muscular atrophy (SMA), resulting in motor circuit defects (1). Loss of TMEM41B in mice results in embryonic lethality (2). TMEM41B is a transmembrane protein that resides at the endoplasmic reticulum (ER) and is found at contact sites between the ER and mitochondria (2). Independent CRISPR screens identified TMEM41B as a novel regulator of autophagy, being structurally and functionally related to VMP1 (3-5). Loss of TMEM41B inhibited autophagosome formation and autophagic flux (3-5). Furthermore, depletion of TMEM41B led to an accumulation of lipid droplets, indicating a role in lipid mobilization and utilization of fatty acids (3,4). TMEM41B also appeared in screens, identifying it as an essential host protein for infection of flaviviruses and coronaviruses, including SARS-CoV-2 (6,7).
    For Research Use Only. Not For Use In Diagnostic Procedures.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.