The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Mechanism of Transdominant Inhibition of CCR5-mediated HIV-1 Infection by ccr5Δ32
Open accessAbstract
Human chemokine receptor 5 (CCR5) functions as a co-receptor for Human immunodeficiency virus (HIV-1) infection. CCR5 is a seven-transmembrane cell surface receptor. Recently, a naturally occurring mutation of CCR5, ccr5Delta32, has been described. A small number of Caucasians are homozygously ccr5Delta32/ccr5Delta32, while a larger number of individuals are heterozygously CCR5/ccr5Delta32. The ccr5Delta32/ccr5Delta32 genotype has been linked to a phenotype that is "highly" protected from HIV-1 infection. On the other hand, several studies have shown that the CCR5/ccr5Delta32 genotype confers "relative" protection from AIDS with onset of disease being delayed by 2-4 years. Although it is known that peripheral blood lymphocytes from heterozygous individuals (CCR5/ccr5Delta32) support ex vivo HIV-1 replication at a reduced level compared with CCR5/CCR5 cells, the molecular basis for this observation is unknown. Here we report on events that post-translationally modify CCR5. We show that CCR5 progresses through the endoplasmic reticulum prior to appearing on the cell surface. Mature CCR5 can be post-translationally modified by phosphorylation and/or co-translationally by multimerization. By contrast, mutant ccr5Delta32, although retaining the capacity for multimerization, was incapable of being phosphorylated. ccr5Delta32 heterocomplexes with CCR5, and this interaction retains CCR5 in the endoplasmic reticulum resulting in reduced cell surface expression. Thus, co-expression in cells of ccr5Delta32 with CCR5 produces a trans-inhibition by the former of ability by the latter to support HIV-1 infection. Taken together, our findings suggest CCR5/ccr5Delta32 heterodimerization as a molecular explanation for the delayed onset of AIDS in CCR5/ccr5Delta32 individuals.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
HIV-1 Entry Cofactor: Functional cDNA Cloning of a Seven-Transmembrane, G Protein-Coupled Receptor
Feng, Y., Broder, C. C., Kennedy, P. E., & Berger, E. A. (1996) · Science · doi:10.1126/science.272.5263.872 · Cited by 4,172
Identification of a major co-receptor for primary isolates of HIV-1
Deng, H., Liu, R., Ellmeier, W., Choe, S., Unutmaz, D., Burkhart, M., Marzio, P. D., Marmon, S., Sutton, R. E., Hill, C. M., et al. (1996) · Nature · doi:10.1038/381661a0 · Cited by 3,641
Improved method for high efficiency transformation of intact yeast cells
Gietz, D., Jean, A. S., Woods, R. A., & Schiestl, R. H. (1992) · Nucleic Acids Research · doi:10.1093/nar/20.6.1425 · Cited by 3,261
HIV-1 entry into CD4+ cells is mediated by the chemokine receptor CC-CKR-5
Dragic, T., Litwin, V., Allaway, G. P., Martin, S. R., Huang, Y., Nagashima, K. A., Cayanan, C., Maddon, P. J., Koup, R. A., Moore, J. P., et al. (1996) · Nature · doi:10.1038/381667a0 · Cited by 3,174
Self-citationLiu, R., Paxton, W. A., Choe, S., Ceradini, D., Martin, S. R., Horuk, R., MacDonald, M. E., Stuhlmann, H., Koup, R. A., & Landau, N. R. (1996) · Cell · doi:10.1016/s0092-8674(00)80110-5 · Cited by 3,074
Self-citationSamson, M., Libert, F., Doranz, B. J., Rucker, J., Liesnard, C., Farber, C.-M., Saragosti, S., Lapouméroulie, C., Cognaux, J., Forceille, C., et al. (1996) · Nature · doi:10.1038/382722a0 · Cited by 2,886
Cocchi, F., DeVico, A. L., Garzino-Demo, A., Arya, S. K., Gallo, R. C., & Lusso, P. (1995) · Science · doi:10.1126/science.270.5243.1811 · Cited by 2,869
CC CKR5: A RANTES, MIP-1α, MIP-1β Receptor as a Fusion Cofactor for Macrophage-Tropic HIV-1
Alkhatib, G., Combadiere, C., Broder, C. C., Feng, Y., Kennedy, P. E., Murphy, P. M., & Berger, E. A. (1996) · Science · doi:10.1126/science.272.5270.1955 · Cited by 2,706
Dean, M., Carrington, M., Winkler, C., Huttley, G. A., Smith, M. W., Allikmets, R., Goedert, J. J., Buchbinder, S. P., Vittinghoff, E., Gomperts, E., et al. (1996) · Science · doi:10.1126/science.273.5283.1856 · Cited by 2,484
The β-Chemokine Receptors CCR3 and CCR5 Facilitate Infection by Primary HIV-1 Isolates
Choe, H., Farzan, M., Sun, Y., Sullivan, N., Rollins, B., Ponath, P. D., Wu, L., Mackay, C. R., LaRosa, G., Newman, W., et al. (1996) · Cell · doi:10.1016/s0092-8674(00)81313-6 · Cited by 2,287
Cited by
Chemokine receptors as HIV-1 coreceptors: roles in viral entry, tropism, and disease
Berger, E. A., Murphy, P. M., & Farber, J. M. (1999) · Annual Review of Immunology · doi:10.1146/annurev.immunol.17.1.657 · Cited by 2,180
International Union of Pharmacology. XXII. Nomenclature for Chemokine Receptors
Murphy, P. M., Baggiolini, M., Charo, I. F., Hébert, C. A., Horuk, R., Matsushima, K., Miller, L. H., Oppenheim, J. J., & Power, C. A. (2000) · Pharmacological Reviews · doi:10.1016/s0031-6997(24)01439-x · Cited by 1,817
The Melanocortin-4 Receptor: Physiology, Pharmacology, and Pathophysiology
Tao, Y.-X. (2010) · Endocrine Reviews · doi:10.1210/er.2009-0037 · Cited by 531
PROKR2 missense mutations associated with Kallmann syndrome impair receptor signalling activity
Monnier, C., Dodé, C., Fabre, L., Teixeira, L., Labesse, G., Pin, J.-P., Hardelin, J.-P., & Rondard, P. (2009) · Human Molecular Genetics · doi:10.1093/hmg/ddn318 · Cited by 123
Targeting CCR5 as a Component of an HIV-1 Therapeutic Strategy
Mohamed, H., Gurrola, T., Berman, R., Collins, M., Sariyer, I. K., Nonnemacher, M. R., & Wigdahl, B. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2021.816515 · Cited by 81
Metadata
- Authors
- Benkirane, M., Jin, D.-Y., Chun, R. F., Koup, R. A., & Jeang, K.-T.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1997-12
- Volume
- 272
- Issue
- 49
- Pages
- 30603-30606
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1966815718
- Cited by
- 377
- References
- 26
- FWCI
- 6.73
- Type
- journal article
- Language
- en
- Open access
- hybrid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Mechanism of Transdominant Inhibition of CCR5-mediated HIV-1 Infection by ccr5Δ32. https://app.cochat.ai/papers/10.1074/jbc.272.49.30603
- The paper
- Benkirane, M., Jin, D.-Y., Chun, R. F., Koup, R. A., & Jeang, K.-T. (1997). Mechanism of Transdominant Inhibition of CCR5-mediated HIV-1 Infection by ccr5Δ32. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.272.49.30603
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
