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> Antibody > Rabbit PAb Antibody > MANF / ARMET Antibody (Antigen Affinity Purified) MANF / ARMET Antibody (Antigen Affinity Purified)
| Catalog | Size (Price) | Quantity | In Stock | Operation | Other Information |
| 11324-RP02 |
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MANF / ARMET Antibody (Antigen Affinity Purified) Datasheet
| Order or Inquire for MANF / ARMET Antibody product | Quality antibodies | Antibody production services | ||
| Detection limit is 0.039 ng/well in ELISA |
MANF / ARMET Antibody Product Information
| Immunogen : |
Recombinant Human MANF / ARMET protein (Catalog#11324-H08H) |
| Antibody Type : | Rabbit Polyclonal Antibody ( Antibody Purification Platform ) |
| Ig Type : |
Rabbit IgG |
| Formulation : | 0.2 μm filtered solution in PBS with 5% trehalose |
| Preparation : |
Produced in rabbits immunized with purified, recombinant Human MANF / ARMET (rh MANF / ARMET; Catalog#11324-H08H; NP_006001.3; Met 1-Leu 179). MANF / ARMET specific IgG was purified by Human MANF / ARMET affinity chromatography. |
MANF / ARMET Antibody Usage Guide
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Specificity : |
Human MANF / ARMET |
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| Western blot : |
This antibody can be used at 5-10 μg/mL with the appropriate secondary reagents to detect Human MANF in WB.
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| Direct ELISA : | This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Human MANF. The detection limit for Human MANF is approximately 0.039 ng/well. | ||||||||||||||||||||
| Storage : | This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free. Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles. |
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MANF / ARMET Antibody Related Products & Topics
Related Areas:
Neuroscience>>Neurotrophic Factor & Receptor>>Other Neurotrophic Factors>>MANF/ARMET
Proteins:
| Molecule | Species | Description //For Detailed Info. and Price------CLICK! | Cat. No |
| MANF/ARMET | Human | MANF/ARMET Protein, Recombinant | 11324-H08H |
| MANF/ARMET | Mouse | MANF / ARMET Protein, Recombinant | 50954-M08H |
Antibodies:
| Molecule | Application | Description //For Detailed Info. and Price------CLICK! | Cat. No |
| Human MANF/ARMET | WB, ELISA | MANF / ARMET Antibody | 11324-RP02 |
MANF / ARMET Antibody Background
Mesencephalic astrocyte-derived neurotrophic factor, also known as Protein ARMET, Arginine-rich protein, MANF and ARMET, is a secreted protein which belongs to theARMET family. ARMET selectively promotes the survival of dopaminergic neurons of the ventral mid-brain. It modulates GABAergic transmission to the dopaminergic neurons of the substantia nigra. ARMET enhances spontaneous, as well as evoked, GABAergic inhibitory postsynaptic currents in dopaminergic neurons. ARMET inhibits cell proliferation and endoplasmic reticulum (ER) stress-induced cell death. The N-terminal region of ARMET may be responsible for neurotrophic activity while the C-terminal region may play a role in the ER stress response. MANF reduces endoplasmic reticulum (ER) stress and has neurotrophic effects on dopaminergic neurons. Intracortical delivery of recombinant MANF protein protects tissue from ischemic brain injury. MANF has been described as a survival factor for dopaminergic neurons. MANF and a homologous protein, the conserved dopamine neurotrophic factor (CDNF), form a novel evolutionary conserved family of neurotrophic factors. MANF expression was widespread in the nervous system and non-neuronal tissues. In the brain, relatively high MANF levels were detected in the cerebral cortex, hippocampus and cerebellar Purkinje cells. The widespread expression of MANF together with its evolutionary conserved nature and regulation by brain insults suggest that it has important functions both under normal and pathological conditions in many tissue types.
References
- Shridhar V., et al., 1996, Oncogene. 12: 1931-1939.
- Gevaert K., et al., 2003, Nat. Biotechnol. 21: 566-569.
- Petrova P., et al., 2003, J. Mol. Neurosci. 20: 173-188.
- Lindholm, P. et al., 2008, Mol Cell Neurosci. 39 (3): 356-71.
- Airavaara, M. et al., 2010, Exp Neurol. 225 (1): 104-13.

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