Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles.
Buffer
Antiserum
Preservative
No Preservative
Concentration
LYOPH
Purity
Unpurified
Reconstitution Instructions
Lyophilized powder, reconstituted in distilled water.
Alternate Names for TMEM49 Antibody
DKFZp566I133
EPG3
TDC1
transmembrane protein 49TMEM49
vacuole membrane protein 1
Background
Transmembrane protein 49 (TMEM49), also known as vacuole membrane protein 1 (VMP1), is an endoplasmic reticulum (ER)-localized protein that plays an important role in autophagy and, specifically, autophagosome formation (1). TMEM49/VMP1 is synthesized as 406 amino acid (aa) transmembrane protein containing a VTT (VMP1-TMEM41b-TVP38) domain and with a theoretical molecular weight of 46 kDa (1,2). TMEM49 helps regulate ER contacts with membranes such as isolation membranes, mitochondria, endosomes, and lipid droplets (1). TMEM49/VMP1 deficiency leads to tighter ER contacts and, in the context of autophagy, results in failure of the autophagosome and lysosome to fuse and eventual disruption of autophagic flux (1).
TMEM49/VMP1 was first implicated in pancreatitis and its overexpression, together with KRAS oncogene activation, leads to development of pancreatic ductal adenocarcinoma (PDAC) (3). Aside from pancreatitis, TMEM49/VMP1 is also associated with a number of other pathologies including cancer, inflammatory bowel disease, and, potentially, neurodegenerative disorders such as Parkinson's Disease (PD) and Alzheimer's Disease (AD) (1). It is suggested that TMEM49/VMP1 deficiency in neurons results in disrupted autophagy and protein aggregation, increased ER-membrane contacts, and dysfunctional mitochondrial homeostasis, all of which contribute to neurodegeneration (1).
References
1. Wang, P., Kou, D., & Le, W. (2020). Roles of VMP1 in Autophagy and ER-Membrane Contact: Potential Implications in Neurodegenerative Disorders. Frontiers in molecular neuroscience, 13, 42. https://doi.org/10.3389/fnmol.2020.00042
2. Uniprot (Q96GC9)
3. Iovanna J. L. (2016). Autophagy Induced during Pancreatitis Promotes KRAS-Dependent Transformation in the Pancreas. Frontiers in oncology, 6, 226. https://doi.org/10.3389/fonc.2016.00226
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
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