Human Fibromodulin HEK293 Overexpression Lysate: Product Information
This Human Fibromodulin overexpression lysate was created in HEK293 Cells and intented for use as a Western blot (WB) positive control. Purification of Fibromodulin protein (Cat: 11514-H02H) from the overexpression lysate was verified.
A DNA sequence encoding the human FMOD (NP_002014.2) (Met1-Ile376) was expressed with the Fc region of human IgG1 at the C-terminus.
The recombinant human FMOD comprises 599 amino acids and has a predicted molecular mass of 68.2 kDa.
Human Fibromodulin HEK293 Overexpression Lysate: Usage Guide
Cell lysate was prepared by homogenization of the over-expressed cells in ice-cold modified RIPA Lysis Buffer with cocktail of protease inhibitors (Sigma). Cell debris was removed by centrifugation. Protein concentration was determined by Bradford assay (Bio-Rad protein assay, Microplate Standard assay). The cell lysate was boiled for 5 min in 1 x SDS loading buffer (50 mM Tris-HCl pH 6.8, 12.5% glycerol, 1% sodium dodecylsulfate, 0.01% bromophenol blue) containing 5% b-mercaptoethanol, and lyophilized.
1. Centrifuge the tube for a few seconds and ensure the pellet at the bottom of the tube.
2. Re-dissolve the pellet using 200μL pure water and boil for 2-5 min.
1 X Sample Buffer (1 X modified RIPA buffer+1 X SDS loading buffer).
Stability & Storage
Store at 4℃ for up to twelve months from date of receipt. After re-dissolution, aliquot and store at -80℃ for up to twelve months. Avoid repeated freeze-thaw cycles.
Western Blot (WB) Optimal dilutions/concentrations should be determined by the end user.
Human Fibromodulin HEK293 Overexpression Lysate: Alternative Names
Human FM Overexpression Lysate; Human SLRR2E Overexpression Lysate
Fibromodulin Background Information
Fibromodulin (FMOD), an ECM small leucine-rich proteoglycan (SLRP), was reported to promote angiogenesis not only during wound healing, but also in optical and cutaneous angiogenesis-dependent diseases. The autocrine FMOD of cancer cells may promote tumor angiogenesis of SCLC by upregulating the expression of angiogenic factors that act in concert to facilitate the angiogenic phenotype of endothelial cells as a proangiogenic factor. Therefore, silencing FMOD may be a potentially clinical therapy for repressing tumor angiogenesis.
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