Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Human Immunodeficiency Virus Protein Tat Induces Synapse Loss via a Reversible Process That Is Distinct from Cell Death

26 Nov 2008

Abstract excerpt

Human immunodeficiency virus (HIV)-1 infection of the CNS produces changes in dendritic morphology that correlate with cognitive decline in patients with HIV-1 associated dementia (HAD). Here, we investigated the effects of HIV-1 transactivator of transcription (Tat), a protein released by virus-infected cells, on synapses between hippocampal neurons using an imaging-based assay that quantified clusters of the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy in Disease and Therapy
Share to HIV Research and Treatment
Share to RNA Interference and Gene Delivery

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 19036954
DOI: 10.1523/jneurosci.2958-08.2008

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Human Immunodeficiency Virus Protein Tat Induces Synapse Loss via a Reversible Process That Is Distinct from Cell DeathPMID 19036954Read ↗

HIV-1 Tat protein variants: critical role for the cysteine region in synaptodendritic injury.Semantic proximity Read ↗

Synaptodendritic injury with HIV-Tat protein: What is the therapeutic target?Semantic proximity Read ↗

Human Synaptic Plasticity Gene Expression Profile and Dendritic Spine Density Changes in HIV-Infected Human CNS Cells: Role in HIV-Associated Neurocognitive Disorders (HAND)Semantic proximity Read ↗

Rapid, concurrent alterations in pre- and postsynaptic structure induced by naturally-secreted amyloid-beta protein.Semantic proximity Read ↗

HIV-1 Tat Induces Dysregulation of PGC1-Alpha and Sirtuin 3 Expression in Neurons: The Role of Mitochondrial Biogenesis in HIV-Associated Neurocognitive Disorder (HAND)Semantic proximity Read ↗

HIV-1 Tat Interactions with p300 and PCAF Transcriptional Coactivators Inhibit Histone Acetylation and Neurotrophin Signaling through CREBSemantic proximity Read ↗

The human immunodeficiency virus type-1 transcription factor Tat produces elevations in intracellular Ca2+ that require function of an N-methyl-D-aspartate receptor polyamine-sensitive site.Semantic proximity Read ↗

Chronic low-level expression of HIV-1 Tat promotes a neurodegenerative phenotype with aging.Semantic proximity Read ↗

Interactions of human immunodeficiency virus‐1 proteins with neurons: possible role in the development of human immunodeficiency virus‐1‐associated dementiaSemantic proximity Read ↗

Distinct domains within PSD-95 mediate synaptic incorporation, stabilization, and activity-dependent trafficking.Semantic proximity Read ↗

Long-term HIV-1 Tat Expression in the Brain Led to Neurobehavioral, Pathological, and Epigenetic Changes Reminiscent of Accelerated AgingSemantic proximity Read ↗

HIV-1 Tat protein exposure alters the morphological characteristics and gene expression in the primary mouse cortex endothelial cells and human brain microvascular endothelial cellsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.