TMEM49 Antibody [Alexa Fluor® 594]

Alexa Fluor (R) products are provided under an intellectual property license from Life Technologies Corporation. The purchase of this product conveys to the buyer the non-transferable right to use the purchased product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components, or any materials made using the product or its components, in any activity to generate revenue, which may include, but is not limited to use of the product or its components: (i) in manufacturing; (ii) to provide a service, information, or data in return for payment; (iii) for therapeutic, diagnostic or prophylactic purposes; or (iv) for resale, regardless of whether they are resold for use in research. For information on purchasing a license to this product for purposes other than as described above, contact Life Technologies Corporation, 5791 Van Allen Way, Carlsbad, CA 92008 USA or outlicensing@lifetech.com. This conjugate is made on demand. Actual recovery may vary from the stated volume of this product. The volume will be greater than or equal to the unit size stated on the datasheet.

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

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.

Array NBP2-78784AF594

• TMEM49 Antibodies
• TMEM49 Proteins