<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-08-29T09:17:28Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/26797" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/26797</identifier><datestamp>2025-12-18T13:01:53Z</datestamp><setSpec>com_20.500.12105_19604</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19605</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Jiménez-Jiménez, Víctor</subfield>
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      <subfield code="a">Sánchez-Cabo, Fátima</subfield>
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      <subfield code="a">Schwartz, Martin A</subfield>
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      <subfield code="a">Sánchez-Álvarez, Miguel</subfield>
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      <subfield code="a">Del Pozo, Miguel Ángel</subfield>
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      <subfield code="a">CAV1 is a protein-coding gene linked to several disorders, including cancer, lipodystrophy, and cardiovascular diseases. While its ability to respond to various mechanical and metabolic stimuli has been documented, a comprehensive understanding of its physiological regulation in humans is lacking. We leveraged the comprehensiveness of human post-mortem tissue data from the Genotype-Tissue Expression (GTEx) consortium, systematically exploring the sources of variability in CAV1 transcriptional levels using extensive bulk and single-nuclei RNA-seq datasets. This human-centric approach, avoiding inter-species comparisons, constitutes a unique resource to explore CAV1 regulation within the complexity of human tissues. Notably, cell type proportion was identified as a major determinant of CAV1 transcription levels across tissues. Donor physiological conditions, including disease states and end-of-life circumstances, also exhibited a tissue-specific influence. Among primary upstream regulators associated with CAV1, chromatin modifiers stood out, especially SMARCA2, which showed a positive correlation across tissues, and PRC2 complexes, which exhibited tissue-specific correlation. Upstream regulatory networks determining CAV1 levels are also enriched for annotations such as mechanobiology (e.g., TEAD4), immunity (e.g., RELA and STAT3), and metabolism (e.g., MYC and NRF1). A remarkable observation was a strong correlation between CAV1 and the relative infiltration of immune cells across tissues, supporting a potential role for CAV1 as a marker and driver of tissue immune infiltration.</subfield>
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      <subfield code="a">Int J Mol Sci. 2025 Apr 17;26(8):3789.</subfield>
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      <subfield code="a">International Journal of Molecular Sciences</subfield>
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      <subfield code="a">40332409</subfield>
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      <subfield code="a">https://hdl.handle.net/20.500.12105/26797</subfield>
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      <subfield code="a">CAV1</subfield>
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      <subfield code="a">A Survey for Human Tissue-Level Determinants of CAV1 Regulation and Function.</subfield>
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