PEBP1 KO cell line available to order. Free of charge wild type control provided.
Epididymis luminal protein 210, Epididymis secretory protein Li 34, Epididymis secretory protein Li 96, HCNP, HCNPpp, HEL 210, HEL S 34, HEL S 96, Hippocampal cholinergic neurostimulating peptide, Neuropolypeptide h3, PBP, PEBP, PEBP1_HUMAN, Phosphatidylethanolamine binding protein, Phosphatidylethanolamine binding protein 1, Prostatic-binding protein, Raf kinase inhibitor protein, Raf kinase inhibitory protein
PEBP1 KO cell line available to order. Free of charge wild type control provided.
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.
Although we aim to provide customers with a homozygous clone, feasibility will be dependent on the biology of the protein. Should only heterozygous edits be achieved, you will be notified of the outcome and be asked to confirm whether the cell line is acceptable. All clones will be accompanied with DNA sequencing data, and the mutation description.
Recommended control: Human wild-type HCT116 cell line (ab288559). Please note a wild-type cell line is not automatically included with a knockout cell line order, if required please add recommended wild-type cell line at no additional cost using the code WILDTYPE-TMTK1.
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our limited use license and patent pages.
Raf kinase inhibitory protein (RKIP) also known as phosphatidylethanolamine-binding protein 1 (PEBP1) is a significant regulatory protein weighing around 21 kDa. It inhibits the RAF/MEK/ERK signaling cascade by binding to Raf-1 kinase. RKIP shows expression in diverse tissues including the brain heart and liver reflecting its widespread influence across various physiological systems.
RKIP interacts with multiple signaling pathways by acting as a suppressor of the mitogen-activated protein kinase (MAPK) pathway. It also plays roles in modulating the signaling of nuclear factor kappa B (NF-κB) and G-protein coupled receptor kinase (GRK) pathways. As part of these pathways RKIP contributes to the regulation of cell proliferation differentiation and apoptosis making it an important player in maintaining cellular homeostasis.
RKIP's role centers on the RAF/MEK/ERK and NF-κB signaling pathways. Within the RAF/MEK/ERK pathway RKIP modulates cellular responses by controlling the activation of Raf-1 influencing cell growth and division. In the NF-κB pathway RKIP inhibits phosphorylation of IKK thereby impacting inflammatory responses which links RKIP to proteins like MEK and ERK as well as IKK.
RKIP has involvement in cancer and cardiovascular diseases. Reduced RKIP expression associates with increased metastasis in cancers such as prostate and breast cancer indicating its role as a metastasis suppressor. In cardiovascular contexts RKIP affects hypertension pathogenesis through the modulation of GRK pathway involving connections to proteins such as Raf-1 and IKK.
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