HPV16 E7

HPV infection is caused by a human papillomavirus, a DNA virus from the papillomavirus family, of which over 150 types are known. More than 40 types are transmitted through sexual contact and infect the anus and genitals Risk factors for persistent HPV infections include early age of first sexual intercourse, multiple partners, smoking, and poor immune function. HPV is typically spread by sustained direct skin-to-skin contact with vaginal and anal sex being the most common methods. Occasionally, it can spread from a mother to her baby during pregnancy. It does not spread via common items like toilet seats. People can become infected with more than one type of HPV. HPV only affects humans. The two primary oncoproteins of high risk HPV types are E6 and E7. The "E" designation indicates that these two proteins are expressed early in the HPV life cycle, while the "L" designation indicates late expression. The HPV genome is composed of six early (E1, E2, E4, E5, E6, and E7) ORFs, two late (L1 and L2) ORFs, and a non-coding long control region (LCR). E7 (in oncogenic HPVs) acts as the primary transforming protein. E7 competes for retinoblastoma protein (pRb) binding, freeing the transcription factor E2F to transactivate its targets, thus pushing the cell cycle forward. All HPV can induce transient proliferation, but only strains 16 and 18 can immortalize cell lines in vitro. It has also been shown that HPV 16 and 18 cannot immortalize primary rat cells alone; there needs to be activation of the ras oncogene.

Human Papilloma virus type 16 early protein E7

Plays a role in viral genome replication by driving entry of quiescent cells into the cell cycle. Stimulation of progression from G1 to S phase allows the virus to efficiently use the cellular DNA replicating machinery to achieve viral genome replication. E7 protein has both transforming and trans-activating activities. Induces the disassembly of the E2F1 transcription factor from RB1, with subsequent transcriptional activation of E2F1-regulated S-phase genes. Interferes with host histone deacetylation mediated by HDAC1 and HDAC2, leading to transcription activation. Plays also a role in the inhibition of both antiviral and antiproliferative functions of host interferon alpha. Interaction with host TMEM173/STING impairs the ability of TMEM173/STING to sense cytosolic DNA and promote the production of type I interferon (IFN-alpha and IFN-beta).

Modulation by virus of host G1/S transition checkpoint Source: UniProtKB-UniRule
Modulation by virus of host transcription Source: UniProtKB
Positive regulation by symbiont of host transcription Source: UniProtKB
Positive regulation of actin filament polymerization Source: UniProtKB
Suppression by virus of host cysteine-type endopeptidase activity involved in apoptotic process Source: UniProtKB
Suppression by virus of host JAK-STAT cascade via inhibition of host IRF9 activity Source: UniProtKB
Suppression by virus of host type I interferon-mediated signaling pathway Source: UniProtKB-UniRule
Transcription, DNA-templated Source: UniProtKB-UniRule

Host cytoplasm; Host nucleus. Predominantly found in the host nucleus.

Highly phosphorylated.