Tropomyosin 3 (TPM3) (NM_153649) Human Tagged ORF Clone Lentiviral Particle

CAT#: RC209904L1V

Lenti ORF particles, TPM3 (Myc-DDK tagged) - Human tropomyosin 3 (TPM3), transcript variant 2, 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Symbol: TPM3
• Synonyms: CAPM1; CFTD; HEL-189; HEL-S-82p; hscp30; NEM1; OK/SW-cl.5; TM-5; TM3; TM5; TM30; TM30nm; TPM3nu; TPMsk3; TRK
• Vector: pLenti-C-Myc-DDK
• ACCN: NM_153649
• ORF Size: 744 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC209904).
• 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_153649.3, NP_705935.1
• RefSeq Size: 3212 bp
• RefSeq ORF: 747 bp
• Locus ID: 7170
• Cytogenetics: 1q21.3
• Domains: Tropomyosin
• Protein Pathways: Cardiac muscle contraction, Dilated cardiomyopathy, Hypertrophic cardiomyopathy (HCM), Pathways in cancer, Thyroid cancer
• MW: 28.9 kDa
• Gene Summary: 'This gene encodes a member of the tropomyosin family of actin-binding proteins. Tropomyosins are dimers of coiled-coil proteins that provide stability to actin filaments and regulate access of other actin-binding proteins. Mutations in this gene result in autosomal dominant nemaline myopathy and other muscle disorders. This locus is involved in translocations with other loci, including anaplastic lymphoma receptor tyrosine kinase (ALK) and neurotrophic tyrosine kinase receptor type 1 (NTRK1), which result in the formation of fusion proteins that act as oncogenes. There are numerous pseudogenes for this gene on different chromosomes. Alternative splicing results in multiple transcript variants. [provided by RefSeq, May 2013]'