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Article

Enhanced function with decreased internalization of carboxy-terminus truncated CXCR4 responsible for WHIM syndrome

22 Mar 2005

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Share to Chemokine receptors and signaling
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 15781337
DOI: 10.1016/j.exphem.2005.01.001

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Related research

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Enhanced function with decreased internalization of carboxy-terminus truncated CXCR4 responsible for WHIM syndromePMID 15781337Read ↗

WHIM syndrome: A defect in CXCR4 signalingSemantic proximity Read ↗

The complex nature of CXCR4 mutations in WHIM syndrome.Semantic proximity Read ↗

WHIM Syndrome: Report of a Novel Familial CXCR4V340fs Gain-of-function Mutation with a Milder PhenotypeSemantic proximity Read ↗

The negative charge of the 343 site is essential for maintaining physiological functions of CXCR4.Semantic proximity Read ↗

Heterogeneous phenotype of a Chinese Familial WHIM syndrome with CXCR4V340fs gain-of-function mutation.Semantic proximity Read ↗

WHIM syndrome caused by a single amino acid substitution in the carboxy-tail of chemokine receptor CXCR4.Semantic proximity Read ↗

CXCR4 mutations in WHIM syndrome: a misguided immune system?Semantic proximity Read ↗

Reduced G protein signaling despite impaired internalization and β-arrestin recruitment in patients carrying a CXCR4Leu317fsX3 mutation causing WHIM syndrome.Semantic proximity Read ↗

CXCR4 signaling in health and disease.Semantic proximity Read ↗

CXCR4 dimerization and beta-arrestin-mediated signaling account for the enhanced chemotaxis to CXCL12 in WHIM syndrome.Semantic proximity Read ↗

A novel transmembrane CXCR4 variant that expands the WHIM genotype-phenotype paradigm.Semantic proximity Read ↗

Genotype–phenotype correlations in WHIM syndrome: a systematic characterization of CXCR4WHIM variantsSemantic proximity Read ↗

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