LATS1 (NM_004690) Human Tagged ORF Clone Lentiviral Particle

SKU RC223650L3V

Lenti ORF particles, LATS1 (Myc-DDK-tagged)-Human LATS, large tumor suppressor, homolog 1 (Drosophila) (LATS1), 200ul, >10^7 TU/mL

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Target Symbol: LATS1
• Synonyms: WARTS; wts
• Vector: pLenti-C-Myc-DDK-P2A-Puro
• Mammalian Cell Selection: Puromycin
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC223650).
• ACCN: NM_004690
• ORF Size: 3390 bp
• OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info
• OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene.
• Shipping: Dry Ice

Reference Data

• RefSeq: NM_004690.2
• RefSeq Size: 4756 bp
• RefSeq ORF: 3393 bp
• Locus ID: 9113
• UniProt ID: O95835
• Cytogenetics: 6q25.1
• Domains: pkinase, UBA
• Protein Families: Druggable Genome, Protein Kinase
• MW: 126.7 kDa
• Summary: 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. [provided by RefSeq, Apr 2017]