| Source: |
Escherichia coli |
| Molecular Weight: |
Approximately 15.8 kDa, a single non-glycosylated polypeptide chain containing 143 amino acids. |
| AA Sequence: |
MVSEPTTVPF DVRPGGVVHS FSQDVGPGNK FTCTFTYASQ GGTNEQWQMS
LGTSEDSQHF TCTIWRPQGK SYLYFTQFKA ELRGAEIEYA MAYSKAAFER
ESDVPLKSEE FEVTKTAVSH RPGAFKAELS KLVIVAKAAR SEL |
| Purity: |
> 95% by SDS-PAGE and HPLC analyses. |
| Physical Appearance: |
Sterile filtered white lyophilized (freeze-dried) powder. |
| Formulation: |
Lyophilized from a 0.2 µm filtered concentrated solution in PBS, pH7.4. |
| Endotoxin: |
Less than 1 EU/µg of rMuSF-20/MYDGF as determined by LAL method. |
| Reconstitution: |
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the
bottom. Reconstitute in sterile distilled water or aqueous buffer containing 0.1% BSA to a
concentration of 0.1-1.0 mg/mL. Stock solutions should be apportioned into working aliquots and
stored at ≤ -20°C. Further dilutions should be made in appropriate buffered solutions. |
| Stability & Storage: |
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
- A minimum of 12 months from date of receipt, when stored at ≤ -20°C as supplied.
- 1 month, 2 to 8°C under sterile conditions after reconstitution.
- 3 months, -20 to -70°C under sterile conditions after reconstitution. |
| Synonyms: |
Il25, Ly6elg, D17Wsu104e |
| Background: |
Myeloid-Derived Growth Factor (MYDGF) is a protein primarily synthesized by bone marrow-derived monocytes and macrophages with the aim of safeguarding and repairing the heart post-myocardial infarction (MI). Although MYDGF shows robust expression in the prostate, spleen, and lung, its presence is relatively subdued in the left ventricle and liver. Notably, its predominant expression occurs in inflammatory cells like monocytes and macrophages, while its presence in neutrophils, T-cells, B-cells, endothelial cells, and cardiac myocytes is comparatively faint at the protein level following MI. During events of ischemia, hypoxia, reperfusion injury in the left ventricle, and adipocyte differentiation, the protein levels of MYDGF surge. MYDGF facilitates endothelial cell proliferation via a signaling pathway mediated by MAPK1/3, STAT3, and CCND1, while simultaneously curbing cardiac myocyte apoptosis through a signaling pathway reliant on PI3K/AKT. |
