Factor IX (F9) (NM_000133) Human Tagged ORF Clone Lentiviral Particle

CAT#: RC219065L4V

Lenti ORF particles, F9 (mGFP-tagged) - Human coagulation factor IX (F9), 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: mGFP
• Symbol: Factor IX
• Synonyms: F9 p22; FIX; HEMB; P19; PTC; THPH8
• Mammalian Cell Selection: Puromycin
• Vector: pLenti-C-mGFP-P2A-Puro
• ACCN: NM_000133
• ORF Size: 1383 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC219065).
• 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.

Reference Data

• RefSeq: NM_000133.2
• RefSeq Size: 2804 bp
• RefSeq ORF: 1386 bp
• Locus ID: 2158
• UniProt ID: P00740
• Cytogenetics: Xq27.1
• Domains: GLA, Tryp_SPc, EGF_CA, EGF, EGF
• Protein Families: Druggable Genome, Protease, Secreted Protein
• Protein Pathways: Complement and coagulation cascades
• MW: 51.78 kDa
• Gene Summary: This gene encodes vitamin K-dependent coagulation factor IX that circulates in the blood as an inactive zymogen. This factor is converted to an active form by factor XIa, which excises the activation peptide and thus generates a heavy chain and a light chain held together by one or more disulfide bonds. The role of this activated factor IX in the blood coagulation cascade is to activate factor X to its active form through interactions with Ca+2 ions, membrane phospholipids, and factor VIII. Alterations of this gene, including point mutations, insertions and deletions, cause factor IX deficiency, which is a recessive X-linked disorder, also called hemophilia B or Christmas disease. Alternative splicing results in multiple transcript variants encoding different isoforms that may undergo similar proteolytic processing. [provided by RefSeq, Sep 2015]