research use only
Cat.No.: F7112
| Dilution |
|---|
|
| Application |
|---|
| WB, IP, IHC |
| Reactivity |
|---|
| Human, Mouse, Rat, Monkey |
| Source |
|---|
| Rabbit Monoclonal Antibody |
| Storage Buffer |
|---|
| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
|---|
| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
|---|
| 73 kDa |
| Specificity |
|---|
| PRMT5 Antibody [M17F9] detects endogenous levels of total PRMT5 protein. |
| Clone |
|---|
| M17F9 |
| Synonym(s) |
|---|
| Protein arginine N-methyltransferase 5; PRMT5; 72 kDa ICln-binding protein; Jak-binding protein 1; Shk1 kinase-binding protein 1 homolog (SKB1 homolog; SKB1Hs); HRMT1L5; IBP72; JBP1; SKB1 |
| Background |
|---|
| PRMT5 (protein arginine methyltransferase 5) is a type II arginine methyltransferase that forms a stable complex with the methyltransferase cofactor WD repeat domain 77 (WDR77/MEP50) and is widely expressed in mammalian cells, where it catalyzes symmetric dimethylation of arginine residues on histones and multiple non‑histone substrates. PRMT5 is incorporated into chromatin remodeling complexes such as SWI/SNF and NuRD and methylates histones H3 and H4, which modulates chromatin compaction and transcriptional repression at specific loci, including genes involved in differentiation and cell‑cycle control. PRMT5 also methylates RNA‑processing factors and transcriptional regulators, thereby influencing pre‑mRNA splicing, export, and the activity of key signaling effectors, and contributes to the regulation of pathways such as p53‑dependent stress responses, translation initiation via eIF4E, and EGFR/Akt/GSK3β signaling in cancer cells. PRMT5 activity is required for G1‑to‑S phase progression, and loss or inhibition of PRMT5 triggers cell‑cycle arrest and reduces expression of cyclins and other growth‑promoting factors, whereas PRMT5 upregulation or aberrant activity is linked to enhanced proliferation and survival in multiple tumors. PRMT5‑dependent methylation modulates interferon and inflammatory signaling in T cells, and PRMT5 inhibition has been shown to blunt interferon‑stimulated gene expression and STAT1 activation, linking it to immune‑cell activation and inflammatory disease. |
| References |
|---|
|
Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.