IL-10-expressing Oncolytic Herpes Simplex Virus 1 (ΔΔICP34.5, ΔΔICP47), CMV-IL-10(Cat#: CyOV-0065XY)

This product is a IL-10 expressing oncolytic herpes simplex virus, which is based on HSV-1 with two copies of both ICP34.5 and ICP47 deleted. ICP34.5 protein, is important for viral replication, viral exit from infected cells, prevention of the premature shut-off of protein synthesis in the infected host, and neurovirulence. ICP47 usually functions to block antigen presentation in HSV-infected cells so its disruption leads to a virus that does not confer on infected tumour cells properties that might protect them from the host's immune system when infected with HSV. This product can be used in oncolytic virotherapy research and further recombinant HSV construction.

Specifications

Family Herpesviridae
Species Herpes simplex virus
Serotype Herpes simplex virus 1
Backbone HSV-1 (ΔΔICP34.5, ΔΔICP47)
Backbone Background Herpes simplex virus 1 and 2 (HSV-1 and HSV-2), also known as human herpesvirus 1 and 2 (HHV-1 and HHV-2), are two members of the human Herpesviridae family, a set of viruses that produce viral infections in the majority of humans. Modified Herpes simplex virus is considered as a potential therapy for cancer and has been extensively clinically tested to assess its oncolytic ability.
Gene Modification ΔΔICP34.5, ΔΔICP47
Promoter CMV
Transgene IL-10
Type of Transgene Cytokine
Related Target/Protein Interleukin 10
Capsid Modification None
Titer >1*10^8 PFU
Related Diseases Glioma

Transgene

Alternative Names IL10, interleukin 10, CSIF; TGIF; GVHDS; IL-10; IL10A
Gene ID 3586

Information

Introduction Interleukin 10 (IL-10), also known as human cytokine synthesis inhibitory factor (CSIF), is an anti-inflammatory cytokine. In humans, interleukin 10 is encoded by the IL10 gene. IL-10 signals through a receptor complex consisting of two IL-10 receptor-1 and two IL-10 receptor-2 proteins. Consequently, the functional receptor consists of four IL-10 receptor molecules. IL-10 binding induces STAT3 signalling via the phosphorylation of the cytoplasmic tails of IL-10 receptor 1 + IL-10 receptor 2 by JAK1 and Tyk2 respectively.

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