Cat. # | Size | Qty. | Price |
---|---|---|---|
26087S | 100 µl |
|
REACTIVITY | H Mk |
SENSITIVITY | Endogenous |
MW (kDa) | 17 |
Source/Isotype | Rabbit IgG |
Product Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
NOTE: Please refer to primary antibody product webpage for recommended antibody dilution.
From sample preparation to detection, the reagents you need for your Western Blot are now in one convenient kit: #12957 Western Blotting Application Solutions Kit
NOTE: Prepare solutions with reverse osmosis deionized (RODI) or equivalent grade water.
Load 20 µl onto SDS-PAGE gel (10 cm x 10 cm).
NOTE: Loading of prestained molecular weight markers (#59329, 10 µl/lane) to verify electrotransfer and biotinylated protein ladder (#7727, 10 µl/lane) to determine molecular weights are recommended.
NOTE: Volumes are for 10 cm x 10 cm (100 cm2) of membrane; for different sized membranes, adjust volumes accordingly.
* Avoid repeated exposure to skin.
posted June 2005
revised June 2020
Protocol Id: 10
Human, Monkey
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu35 of human SSBP1 protein.
The mitochondrial DNA replisome requires the activity of single-stranded DNA-binding protein (SSBP1, mtSSB), DNA Polymerase γ (POLG), and the mitochondrial DNA helicase (twinkle/PEO1) (1). SSBP1 enhances the functions of both POLG and PEO1 by binding to and stabilizing single-stranded DNA at the replication fork; knockdown of SSBP1 in vitro causes a gradual depletion of mitochondrial DNA and an acute depletion of 7S DNA (2). Mutations in SSBP1 underlie a variety of disorders, including optic atrophy, nephropathy (3), Pearson syndrome, Leigh syndrome, and Kearns-Sayre syndrome (4-6). SSBP1 has emerged as a potential therapeutic target for glioblastoma (7) and non-small cell lung cancer (NSCLC) (8), as controlled depletion of SSBP1 increases mitochondrial reactive oxygen species (ROS) and sensitizes these cancer cells to temozolomide and radiation therapy, respectively (7,8). The increase in mitochondrial ROS observed with SSBP1 depletion is linked to a corresponding decrease in nuclear ROS (9). ROS-sensing kinase Chk1 phosphorylates SSBP1 at Ser67, causing SSBP1 sequestration in the cytoplasm and limiting the translation of mitochondrial genes (9). This pathway may confer resistance to platinum-based therapies in ovarian cancers (9).
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