Caprin1 (E9F9I) Rabbit mAb #18553
- WB
Supporting Data
| REACTIVITY | H Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 116 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Simple Western™ | 1:10 - 1:50 |
Storage
Protocol
Specificity / Sensitivity
Caprin1 (E9F9I) Rabbit mAb recognizes endogenous levels of total caprin1 protein.
Species Reactivity:
Human, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu201 of human caprin1 protein.
Background
Cytoplasmic activation- and proliferation-associated protein 1 (caprin1) is a ubiquitously expressed RNA binding protein (RBP) that plays an important role in cell cycle regulation. Caprin1 is primarily localized to the cytoplasm and interacts with mRNA through its C-terminal RGG motifs (1). Caprin1 interacts with a variety of mRNA involved in cell cycle regulation, including c-Myc and cyclin D2 (1,2). Additionally, knockout of caprin1 reduces cell proliferation by delaying the transition from the G1 to the S phase of the cell cycle (3). Misregulation of the cell cycle suggests a potential tumorigenic role for caprin1, and its overexpression has been found to promote tumor growth and metastasis in osteosarcoma through interaction with Cyr61 (4). Caprin1 is also known to phase separate and localize to specific RNA granules called stress granules (SGs). SGs are cytoplasmic mRNA-protein condensates that are formed in response to cellular stressors, such as oxidative stress, ultraviolet radiation, and viral infection (5). Caprin1 is a key mediator of SG formation along with the proteins G3BP1 and USP10 (6,7). SG formation is a reversible process under normal physiological conditions, but chronic stress can disrupt SG dissolution and lead to the aggregation of proteins linked to various neurodegenerative diseases (8). Indeed, a missense P512L mutation in the CAPRIN1 gene has been linked to early-onset ataxia, potentially through a gain-of-function mechanism that promotes protein aggregation (9).
- Solomon, S. et al. (2007) Mol Cell Biol 27, 2324-42.
- Qiu, Y.Q. et al. (2015) Oncotarget 6, 2148-63.
- Wang, B. et al. (2005) J Immunol 175, 4274-82.
- Sabile, A.A. et al. (2013) Biochim Biophys Acta 1832, 1173-82.
- Riggs, C.L. et al. (2020) J Cell Sci 133, jcs242487. doi: 10.1242/jcs.242487.
- Kedersha, N. et al. (2016) J Cell Biol 212, 845-60.
- Song, D. et al. (2022) Proc Natl Acad Sci USA 119, e2207975119.
- Wolozin, B. and Ivanov, P. (2019) Nat Rev Neurosci 20, 649-666.
- Delle Vedove, A. et al. (2022) Cell Mol Life Sci 79, 526.
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