Vpr protein: Difference between revisions

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=== Vpr induce cell cycle arrest by recruits cellular targets for degradation<ref>PMID:27571178</ref> ===

One phenotype of Vpr expression is the induction of cell cycle arrest in G2 phase. This arrest executes by engaging of DNA damage–binding protein 1 (DDB1) and CUL4A-associated factor 1 (DCAF1) to Vpr. DCAF1 is a substrate receptor of the Cullin4–RING E3 ubiquitin ligase (CRL4) of the host ubiquitin–proteasome-mediated protein degradation pathway. Mutations in Vpr that abolish its interaction with DCAF1, or silencing of DCAF1, eliminate cell-cycle arrest.

One phenotype of Vpr expression is the induction of cell cycle arrest in G2 phase. This arrest executes by engaging of DNA damage–binding protein 1 (DDB1) and CUL4A-associated factor 1 (DCAF1) to Vpr. DCAF1 is a substrate receptor of the Cullin4–RING E3 ubiquitin ligase (CRL4) of the host ubiquitin–proteasome-mediated protein degradation pathway. Mutations in Vpr that abolish its interaction with DCAF1, or silencing of DCAF1, eliminate cell-cycle arrest. The crystal structure of DDB1–DCAF1–HIV-1–Vpr–uracil-DNA glycosylase (UNG2) complex elucidate the molecular mechanism in which Vpr inhibits DDB1 enzymatic activity and send it for degradation.

* Vpr binding to the DCAF1 WD40 by its N-terminus and α3 helix. <br/>

* Vpr uses structural mimicry to DNA to engages UNG2. <br/>

* DCAF1 is anchored into DDB1 by a helix-loop-helix motif <br/>

== Disease ==

HIV-1 retrovirus is the cause of AIDS disease. HIV-1 is a RNA virus which copy its genome to the host-cell genome in infect cells. HIV-1 infects activated CD4 immune cells and macrophages. When the disease is expressing in carriers, the progressive depletion of CD4 T cells causes immunodeficiency<ref name='Emerman1996'>PMID:8805364</ref>.

Vpr protein: Difference between revisions

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@@ Line 5: / Line 5: @@
 === Vpr induce cell cycle arrest by recruits cellular targets for degradation<ref>PMID:27571178</ref> ===
-One phenotype of Vpr expression is the induction of cell cycle arrest in G2 phase. This arrest executes by engaging of DNA damage–binding protein 1 (DDB1) and CUL4A-associated factor 1 (DCAF1) to Vpr. DCAF1 is a substrate receptor of the Cullin4–RING E3 ubiquitin ligase (CRL4) of the host ubiquitin–proteasome-mediated protein degradation pathway. Mutations in Vpr that abolish its interaction with DCAF1, or silencing of DCAF1, eliminate cell-cycle arrest.
+One phenotype of Vpr expression is the induction of cell cycle arrest in G2 phase. This arrest executes by engaging of DNA damage–binding protein 1 (DDB1) and CUL4A-associated factor 1 (DCAF1) to Vpr. DCAF1 is a substrate receptor of the Cullin4–RING E3 ubiquitin ligase (CRL4) of the host ubiquitin–proteasome-mediated protein degradation pathway. Mutations in Vpr that abolish its interaction with DCAF1, or silencing of DCAF1, eliminate cell-cycle arrest. The crystal structure of DDB1–DCAF1–HIV-1–Vpr–uracil-DNA glycosylase (UNG2) complex elucidate the molecular mechanism in which Vpr inhibits DDB1 enzymatic activity and send it for degradation.
+* Vpr binding to the DCAF1 WD40 by its N-terminus and α3 helix. <br/>
+* Vpr uses structural mimicry to DNA to engages UNG2. <br/>
+* DCAF1 is anchored into DDB1 by a helix-loop-helix motif <br/>
 == Disease ==
 HIV-1 retrovirus is the cause of AIDS disease. HIV-1 is a RNA virus which copy its genome to the host-cell genome in infect cells. HIV-1 infects activated CD4 immune cells and macrophages. When the disease is expressing in carriers, the progressive depletion of CD4 T cells causes immunodeficiency<ref name='Emerman1996'>PMID:8805364</ref>.