Description
LATS1 Antibody | 22-749 | Gentaur UK, US & Europe Distribution
Host: Rabbit
Reactivity: Human, Mouse, Rat
Homology: N/A
Immunogen: Recombinant protein of human LATS1
Research Area: Apoptosis, Cancer, Cell Cycle, Chemokines & Cytokines, Immunology, Signal Transduction
Tested Application: WB, IHC
Application: WB: 1:500 - 1:2000
IHC: 1:50 - 1:200
Specificiy: N/A
Positive Control 1: K-562
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: Observed: 130kDa
Validation: N/A
Isoform: N/A
Purification: Affinity purification
Clonality: Polyclonal
Clone: N/A
Isotype: IgG
Conjugate: Unconjugated
Physical State: Liquid
Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.
Concentration: N/A
Storage Condition: Store at -20˚C. Avoid freeze / thaw cycles.
Alternate Name: WARTS, wts, serine/threonine-protein kinase LATS1, LATS (large tumor suppressor, Drosophila) homolog 1, LATS, large tumor suppressor, homolog 1, WARTS protein kinase, h-warts, large tumor suppressor homolog 1
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: The protein encoded by this gene is a putative serine/threonine kinase that localizes to the mitotic apparatus and complexes with cell cycle controller CDC2 kinase in early mitosis. The protein is phosphorylated in a cell-cycle dependent manner, with late prophase phosphorylation remaining through metaphase. The N-terminal region of the protein binds CDC2 to form a complex showing reduced H1 histone kinase activity, indicating a role as a negative regulator of CDC2/cyclin A. In addition, the C-terminal kinase domain binds to its own N-terminal region, suggesting potential negative regulation through interference with complex formation via intramolecular binding. Biochemical and genetic data suggest a role as a tumor suppressor. This is supported by studies in knockout mice showing development of soft-tissue sarcomas, ovarian stromal cell tumors and a high sensitivity to carcinogenic treatments.