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Manuel Llano

Researcher at University of Texas at El Paso

Publications -  55
Citations -  6808

Manuel Llano is an academic researcher from University of Texas at El Paso. The author has contributed to research in topics: Integrase & Receptor. The author has an hindex of 29, co-authored 53 publications receiving 6440 citations. Previous affiliations of Manuel Llano include Autonomous University of Madrid & Mayo Clinic.

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HLA-E is a major ligand for the natural killer inhibitory receptor CD94/NKG2A.

TL;DR: Examination of HLA-E antigen distribution indicated that it is detectable on the surface of a wide variety of cell types, consistent with the prediction that the ligand for CD94/NKG2A is expressed ubiquitously.
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A Common Inhibitory Receptor for Major Histocompatibility Complex Class I Molecules on Human Lymphoid and Myelomonocytic Cells

TL;DR: A novel inhibitory MHC class I receptor of the immunoglobulin-superfamily is characterized, expressed not only by subsets of NK and T cells, but also by B cells, monocytes, macrophages, and dendritic cells, suggesting that diverse leukocyte lineages have adopted recognition of self–MHC class II molecules as a common strategy to control cellular activation during an immune response.
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A role for LEDGF/p75 in targeting HIV DNA integration.

TL;DR: LEDGF is the first example of a cellular protein controlling the location of HIV integration in human cells and it is found that integration was less frequent in transcription units, lessrequent in genes regulated by LEDGF/p75 and more frequent in GC-rich DNA.
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An essential role for LEDGF/p75 in HIV integration.

TL;DR: Fractionally minute levels of endogenous p75 are sufficient to enable integration and show that cellular factors that engage HIV after entry may elude identification in less intensive knockdowns, showing that p75-integrase interaction may have therapeutic potential.
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HLA-E-bound peptides influence recognition by inhibitory and triggering CD94/NKG2 receptors: preferential response to an HLA-G-derived nonamer

TL;DR: The results raise the possibility that CD94/NKG2‐mediated recognition of HLA‐E expressed on extravillous cytotrophoblasts plays an important role in maternal‐fetal cellular interactions.