Recombinant Human papillomavirus type 16 Protein E7(E7)

$154.00
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Product Code
CSB-EP365855HML
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Product Code: CSB-EP365855HML
Size: 10μg/50μg/100μg/200μg/500μg/1mg
Species of origin: Human papillomavirus type 16
Application: SDS-PAGE
Express system: E.coli
More Information
Uniprot NO. P03129
Target/Protein E7
Species of origin Human papillomavirus type 16
AA Sequence MHGDTPTLHEYMLDLQPETTDLYCYEQLNDSSEEEDEIDGPAGQAEPDRAHYNIVTFCCKCDSTLRLCVQSTHVDIRTLEDLLMGTLGIVCPICSQKP
Biologically Active Not Test
Nature Recombinant
Protein length Full Length
MW of Fusion Proten 15 kDa
Expression Region 1-98aa
Expression System E.coli
Purity Greater than 90% as determined by SDS-PAGE.
Application SDS-PAGE
Tag info N-terminal 6xHis-tagged
Storage The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Reference The N-terminal module of HPV16 E7 is an intrinsically disordered domain that confers conformational and recognition plasticity to the oncoprotein.Garcia-Alai M.M., Alonso L.G., de Prat-Gay G.Biochemistry 46:10405-10412(2007)
Relevance E7 protein has both transforming and trans-activating activities. Disrupts the function of host retinoblastoma protein RB1/pRb, which is a key regulator of the cell cycle. Induces the disassbly of the E2F1 transcription factors from RB1, with subsequent transcriptional activation of E2F1-regulated S-phase genes. Inactivation of the ability of RB1 to arrest the cell cycle is critical for cellular transformation, uncontrolled cellular growth and proliferation induced by viral infection. Stimulation of progression from G1 to S phase allows the virus to efficiently use the cellular DNA replicating machinery to achieve viral genome replication. Interferes with histone deacetylation mediated by HDAC1 and HDAC2, leading to activation of transcription .
Research areas Epigenetics and Nuclear Signaling

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