This Rabbit Polyclonal antibody specifically detects LATS1 in WB and IHC (p). It exhibits reactivity toward Human, Mouse and Ratand has been mentioned in 1 publication.
This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.
Immunogen
This LATS1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1-30 amino acids from the N-terminal region of human LATS1.
LATS1
Reactivity: Human
Host: Rabbit
Polyclonal
FITC
Application Notes
WB: 1:1000. IHC-P: 1:50~100
Restrictions
For Research Use only
Format
Liquid
Buffer
Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.
Preservative
Sodium azide
Precaution of Use
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
4 °C,-20 °C
Storage Comment
Maintain refrigerated at 2-8 °C for up to 6 months. For long term storage store at -20 °C in small aliquots to prevent freeze-thaw cycles.
Expiry Date
6 months
Eiring, Neviani, Santhanam, Oaks, Chang, Notari, Willis, Gambacorti-Passerini, Volinia, Marcucci, Caligiuri, Leone, Perrotti: "Identification of novel posttranscriptional targets of the BCR/ABL oncoprotein by ribonomics: requirement of E2F3 for BCR/ABL leukemogenesis." in: Blood, Vol. 111, Issue 2, pp. 816-28, (2008) (PubMed).
Target
LATS1
(LATS, Large Tumor Suppressor, Homolog 1 (Drosophila) (LATS1))
Alternative Name
LATS1
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.