Form
Liquid
Buffer
0.02M Potassium Phosphate, 0.15M NaCl
Preservative
0.01% Sodium azide
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
Concentration
0.9 mg/ml (Please refer to the vial label for the specific concentration.)
Antigen Species
Human
Immunogen
This affinity purified antibody was prepared from whole rabbit serum produced by repeated immunizations with a synthetic peptide corresponding to amino acids surrounding Thr78 of human MLF1IP protein. ?The immunogen peptide is phosphorylated at Thr78.
Purification
Affinity purified using phosphopeptide and cross-adsorbed against non-phosphorylated peptide
Conjugation
Unconjugated
Note
For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.
Synonyms
centromere protein U , CENP50 , CENPU50 , KLIP1 , MLF1IP , PBIP1
Cellular Localization
Cytoplasm,Nucleus
Background
Myeloid leukemia factor-1 (MLF1) Interacting Protein (also known as PBIP1, MLF1IP1, KLIP1 or KSHV latent nuclear antigen interacting protein 1) is a novel polo-like kinase 1 (Plk1) substrate. Plk1 phosphorylation of MLF1IP induces ubiquitination and degradation of MLF1IP prior to the metaphase/ anaphase transition. Several Plk1-dependent phosphorylation sites have been identified on MLF1IP by mass spectrometry. Mutations of these sites stabilize MLF1IP and inhibit mitotic progression. Subsequent in vitro and in vivo MLF1IP phosphorylation and stability assays have revealed that phosphorylation of Thr78 is critical for triggering Plk1-dependent MLF1IP degradation. Expression of a non-degradable Thr78Ala mutant was sufficient to induce a mitotic block. Timely phosphorylation of MLF1IP on Thr78 by Plk1 is critical for eliminating the MLF1IP-imposed mitotic block prior to anaphase onset. MLF1IP is speculated to be a novel tumor suppressor.
Database
Research Area