Envelope and long terminal repeat sequences of a cloned infectious NZB xenotropic murine leukemia virus

O'Neill, Raymond; Buckler, Charles E.; Theodore, T S; Martin, Malcolm A.; Repaske, Roy

doi:10.1128/jvi.53.1.100-106.1985

Cited by 101 publications

(59 citation statements)

References 46 publications

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“…Additionally, NZB mice express high levels of Xmv mRNA from both constitutive and inducible Xmv loci (Elder et al, 1980). Unlike B6J mice, which predominantly express Xmv9, Xmv10, Xmv13, Xmv14 (all PBS Gln ) and Xmv43 (PBS Pro ) ( Figure 1B & 1D), the highly expressed NZB Xmv NEERV encode PBS Pro (Baudino et al, 2008;O'Neill et al, 1985). Xmv loci can be further subdivided into 4 subgroups, Xmv-I through Xmv-IV, whose transcripts can be amplified with subgroup-specific envelope primers.…”

Section: Snerv1 But Not Snerv2 Strongly Recruits Kap1 and Selectivementioning

confidence: 99%

The lupus susceptibility locus Sgp3 encodes the suppressor of endogenous retrovirus expression SNERV

Treger

Pope

Kong

et al. 2018

Preprint

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Elevated endogenous retrovirus (ERV) transcription and anti-ERV antibody reactivity are implicated in lupus pathogenesis. Overproduction of non-ecotropic ERV (NEERV) envelope glycoprotein, gp70, and resultant nephritis occur in lupus-prone mice. However, a NEERV repressor has not been identified to test if this association is causal. Here we identified suppressor of NEERV (Snerv) 1 & 2, Krüppel-associated box zinc finger proteins (KRAB-ZFP) that repressed NEERV by binding the NEERV long terminal repeat to recruit the transcriptional regulator KAP1. Germline Snerv1/2 deletion increased activating chromatin modifications, transcription, and gp70 expression from NEERV loci. F1 crosses of lupus-prone NZB and 129 mice to Snerv1/2 -/mice failed to restore NEERV repression, demonstrating that loss of SNERV underlies the lupus autoantigen gp70 overproduction that promotes nephritis in susceptible mice. Increased ERV expression in lupus patients was inversely correlated with expression of three putative ERV-suppressing KRAB-ZFP, suggesting that KRAB-ZFP-mediated ERV misexpression may contribute to human lupus pathogenesis.

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Section: Snerv1 But Not Snerv2 Strongly Recruits Kap1 and Selectivementioning

confidence: 99%

The lupus susceptibility locus Sgp3 encodes the suppressor of endogenous retrovirus expression SNERV

Treger

Pope

Kong

et al. 2018

Preprint

View full text Add to dashboard Cite

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“…This implies either that the M-MuLV NED does not form analogous close contact interactions with the viral LTR, or that the M-MuLV viral LTR forms an altered or bent structure, possibly associated with the highly conserved GGGG sequence at positions 10-13 nucleotides upstream of the viral termini that undergoes strand transfer. [44][45][46] Additional positions within the NTR of PFV IN have been identified to be in contact with DNA. These include residues G68, R69, N84, R86, N106, and K107.…”

Section: Structural and Functional Comparison With Pfv In-ntd And Hivmentioning

confidence: 99%

X‐ray crystal structure of the N‐terminal region of Moloney murine leukemia virus integrase and its implications for viral DNA recognition

et al. 2017

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The retroviral integrase (IN) carries out the integration of a dsDNA copy of the viral genome into the host DNA, an essential step for viral replication. All IN proteins have three general domains, the N-terminal domain (NTD), the catalytic core domain (CCD), and the C-terminal domain (CTD). The NTD includes an HHCC zinc finger-like motif, which is conserved in all retroviral IN proteins. Two crystal structures of Moloney murine leukemia virus (M-MuLV) IN N-terminal region (NTR) constructs that both include an N-terminal extension domain (NED, residues 1-44) and an HHCC zinc-finger NTD (residues 45-105), in two crystal forms are reported. The structures of IN NTR constructs encoding residues 1-105 (NTR1-105) and 8-105 (NTR8-105) were determined at 2.7 and 2.15 Å resolution, respectively and belong to different space groups. While both crystal forms have similar protomer structures, NTR1-105 packs as a dimer and NTR8-105 packs as a tetramer in the asymmetric unit. The structure of the NED consists of three anti-parallel β-strands and an α-helix, similar to the NED of prototype foamy virus (PFV) IN. These three β-strands form an extended β-sheet with another β-strand in the HHCC Zn2+ binding domain, which is a unique structural feature for the M-MuLV IN. The HHCC Zn2+ binding domain structure is similar to that in HIV and PFV INs, with variations within the loop regions. Differences between the PFV and MLV IN NEDs localize at regions identified to interact with the PFV LTR and are compared with established biochemical and virological data for M-MuLV.

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“…A vaccinia virus transfer vector used for the expression of the mouse retrovirus env gene was constructed as described previously [22][23][24]. Plasmid clone pNZB 9-1 [25] containing the whole permuted infectious molecular clone of an NZB xenotropic virus, IU-6, was used as the source of endogenous xenotropic virus env gene sequence. The HincII-SmaI fragment harbouring the entire env gene and portions of the pol and LTR from pNZB 9-1 was reconstructed in pBluescript-KS(þ) vector from purified HincII-EcoRI and EcoRI-SmaI fragments, and the unique AccI site upstream of the env initiation codon was replaced with a BamHI linker.…”

Section: Expression Of the Murine Leukaemia Viral Env Gene In A Recommentioning

confidence: 99%

Induction of microthrombotic thrombocytopenia in normal mice by transferring a platelet-reactive, monoclonal anti-gp70 autoantibody established from MRL/lprmice: an autoimmune model of thrombotic thrombocytopenic purpura

Hashimoto

Tabata²,

Fujisawa

et al. 2000

Clinical and Experimental Immunology

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SUMMARYMRL/MpJ-lpr/lpr (MRL/lpr) mice spontaneously develop immune complex-mediated glomerulonephritis and thrombocytopenia. Although the presence of cross-reactive anti-phospholipid antibodies in sera of MRL/lpr mice has been demonstrated, possible relationships between detected autoantibodies and the development of thrombocytopenia have not been elucidated. Recent genetic analyses in a few different strains of lupus-prone mice have pointed out a close correlation between autoantibodies reactive with endogenous retroviral env gene product, gp70, and the development and severity of glomerulonephritis. In the process of establishing possibly nephritogenic anti-gp70 autoantibodyproducing hybridoma cells from MRL/lpr mice, we identified an IgG2a-producing anti-gp70 hybridoma clone that induced microvascular intraluminal platelet aggregation, thrombocytopenia, and amenia upon transplantation into syngeneic non-autoimmune mice. This and two other anti-gp70 antibodies bound onto the surface of mouse platelets, and purified IgG2a of the anti-gp70 autoantibody induced glomerular lesions with characteristics of thrombotic thrombocytopenic purpura when injected into non-autoimmune mice. The pathogenic anti-gp70 autoantibody specifically precipitated a platelet protein with an approximate relative molecular mass of 40 000.

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Envelope and long terminal repeat sequences of a cloned infectious NZB xenotropic murine leukemia virus

Cited by 101 publications

References 46 publications

The lupus susceptibility locus Sgp3 encodes the suppressor of endogenous retrovirus expression SNERV

The lupus susceptibility locus Sgp3 encodes the suppressor of endogenous retrovirus expression SNERV

X‐ray crystal structure of the N‐terminal region of Moloney murine leukemia virus integrase and its implications for viral DNA recognition

Induction of microthrombotic thrombocytopenia in normal mice by transferring a platelet-reactive, monoclonal anti-gp70 autoantibody established from MRL/lprmice: an autoimmune model of thrombotic thrombocytopenic purpura

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