FEN1 Antibody (monoclonal) (M01A)
Mouse monoclonal antibody raised against a partial recombinant FEN1.
- 产品详情
- 实验流程
- 背景知识
Application ![]()
| WB |
---|---|
Primary Accession | P39748 |
Other Accession | NM_004111 |
Reactivity | Human |
Host | mouse |
Clonality | monoclonal |
Isotype | IgM Kappa |
Clone Names | 1E3 |
Calculated MW | 42593 Da |
Gene ID | 2237 |
---|---|
Other Names | Flap endonuclease 1 {ECO:0000255|HAMAP-Rule:MF_03140}, FEN-1 {ECO:0000255|HAMAP-Rule:MF_03140}, 31-- {ECO:0000255|HAMAP-Rule:MF_03140}, DNase IV, Flap structure-specific endonuclease 1 {ECO:0000255|HAMAP-Rule:MF_03140}, Maturation factor 1, MF1, hFEN-1, FEN1 {ECO:0000255|HAMAP-Rule:MF_03140}, RAD2 |
Target/Specificity | FEN1 (NP_004102, 1 a.a. ~ 110 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. |
Dilution | WB~~1:500~1000 |
Format | Clear, colorless solution in phosphate buffered saline, pH 7.2 . |
Storage | Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. |
Precautions | FEN1 Antibody (monoclonal) (M01A) is for research use only and not for use in diagnostic or therapeutic procedures. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The protein encoded by this gene removes 5' overhanging flaps in DNA repair and processes the 5' ends of Okazaki fragments in lagging strand DNA synthesis. Direct physical interaction between this protein and AP endonuclease 1 during long-patch base excision repair provides coordinated loading of the proteins onto the substrate, thus passing the substrate from one enzyme to another. The protein is a member of the XPG/RAD2 endonuclease family and is one of ten proteins essential for cell-free DNA replication. DNA secondary structure can inhibit flap processing at certain trinucleotide repeats in a length-dependent manner by concealing the 5' end of the flap that is necessary for both binding and cleavage by the protein encoded by this gene. Therefore, secondary structure can deter the protective function of this protein, leading to site-specific trinucleotide expansions. [provided by RefSeq]

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