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ELK Biotechnology
SKU:ES2704
LATS1/2 rabbit pAb
LATS1/2 rabbit pAb
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Applications: WB;IHC;IF;ELISA
Reactivity: Human;Mouse
Source: Rabbit
Dilution: Western Blot: 1/500 - 1/2000. IHC-p: 1:100-300 ELISA: 1/20000. IF 1:100-300 Not yet tested in other applications.
Immunogen: The antiserum was produced against synthesized peptide derived from human LATS1/2. AA range:1041-1090
Storage_stability: -20°C/1 year
Clonality: Polyclonal
Isotype: IgG
Concentration: 1 mg/ml
Observed_band(KD): 130-140kD
Human_gene_id: 9113/26524
Human_swiss_prot_no: O95835/Q9NRM7
Subcellular_location: Cytoplasm, cytoskeleton, microtubule organizing center, centrosome . Cytoplasm, cytoskeleton, spindle . Midbody . Cytoplasm, cytoskeleton, microtubule organizing center, spindle pole body . Localizes to the centrosomes throughout interphase but migrates to the mitotic apparatus, including spindle pole bodies, mitotic spindle, and midbody, during mitosis. .
Other_name: LATS1; WARTS; Serine/threonine-protein kinase LATS1; Large tumor suppressor homolog 1; WARTS protein kinase; h-warts; LATS2; KPM; Serine/threonine-protein kinase LATS2; Kinase phosphorylated during mitosis protein; Large tumor suppressor ho
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 treatmen
Reactivity: Human;Mouse
Source: Rabbit
Dilution: Western Blot: 1/500 - 1/2000. IHC-p: 1:100-300 ELISA: 1/20000. IF 1:100-300 Not yet tested in other applications.
Immunogen: The antiserum was produced against synthesized peptide derived from human LATS1/2. AA range:1041-1090
Storage_stability: -20°C/1 year
Clonality: Polyclonal
Isotype: IgG
Concentration: 1 mg/ml
Observed_band(KD): 130-140kD
Human_gene_id: 9113/26524
Human_swiss_prot_no: O95835/Q9NRM7
Subcellular_location: Cytoplasm, cytoskeleton, microtubule organizing center, centrosome . Cytoplasm, cytoskeleton, spindle . Midbody . Cytoplasm, cytoskeleton, microtubule organizing center, spindle pole body . Localizes to the centrosomes throughout interphase but migrates to the mitotic apparatus, including spindle pole bodies, mitotic spindle, and midbody, during mitosis. .
Other_name: LATS1; WARTS; Serine/threonine-protein kinase LATS1; Large tumor suppressor homolog 1; WARTS protein kinase; h-warts; LATS2; KPM; Serine/threonine-protein kinase LATS2; Kinase phosphorylated during mitosis protein; Large tumor suppressor ho
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 treatmen
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