Results 91 to 100 of about 599,394 (294)

Schematic representation of the chemokine receptors CCR5 and CXCR4 and the chimeric CCR5/CXCR4 receptors.

open access: yes, 2013
Chimeric receptors FC-1, FC-2, FC-4b, FC-5, FC-6 and FC-7 were obtained by replacing successively larger parts of CCR5 with corresponding regions of CXCR4.
Marisa Zanchetta (309064)   +8 more
core   +1 more source

HETERODIMERIZATION BETWEEN CHEMOKINE RECEPTORS CXCR4 AND CCR7 AND ITS ROLE IN CANCER [PDF]

open access: yes, 2022
In physiology, the functional and physical interactions between cell surface receptors for signal molecules such as hormones, neurotransmitters, and cytokines, provides an important mechanism of diversity and regulation of signal transduction. Therefore,
Tariq, Maryam Naveed Muhammad
core  

Dual Lineages of Langerhans Cells Cooperate to Restore the Immune Barrier after Skin Injury

open access: yesAdvanced Science, EarlyView.
After skin injury, the epidermal immune barrier is rebuilt by two sources of Langerhans cells. Resident Langerhans cells first move into the wound during re‐epithelialization, guided by CXCR2 signaling. Later, recruited monocytes become long‐lived Langerhans cells.
Axel D. Schmitter‐Sánchez   +8 more
wiley   +1 more source

The complex nature of CXCR4 mutations in WHIM syndrome

open access: yesFrontiers in Immunology
Heterozygous autosomal dominant mutations in the CXCR4 gene cause WHIM syndrome, a severe combined immunodeficiency disorder. The mutations primarily affect the C-terminal region of the CXCR4 chemokine receptor, specifically several potential ...
José Miguel Rodríguez-Frade   +4 more
doaj   +1 more source

MicroRNA 139-5p coordinates APLNR-CXCR4 crosstalk during vascular maturation

open access: yesNature Communications, 2016
G protein-coupled receptors APLNR and CXCR4 are crucial for vascular development. Here, the authors show that these two signaling pathways communicate and that in response to blood flow APLNR signaling induces a decrease in CXCR4 expression via miR-139 ...
Irinna Papangeli   +13 more
doaj   +1 more source

RGS16 Aggravates Hepatic Ischemia‐Reperfusion Injury via Hepatocyte‐Intrinsic Apoptosis/Inflammation & Neutrophil Recruitment/NETosis

open access: yesAdvanced Science, EarlyView.
RGS16 competitively interferes with the YTHDF3–PAN3 complex to prevent CXCL1 mRNA decay during hepatic ischemia‐reperfusion injury. Stabilized CXCL1 strengthens hepatocyte injury, neutrophil recruitment, and NET‐associated inflammation, uncovering how stress‐induced RGS16 converts post‐transcriptional regulation into immune‐mediated liver damage ...
Xinglong Li   +16 more
wiley   +1 more source

Targeting the chemokine receptor CXCR4 for cancer therapies

open access: yesBiomarker Research
Abstract The C-X-C chemokine receptor type 4 (CXCR4) has emerged as a key molecular biomarker for cancer therapies due to its critical role in tumor progression and metastases by displaying a stem cells phenotype. Its overexpression has been observed in more than 20 types of cancers, including solid tumors and hematological malignancies, and ...
Ariana Rueda   +4 more
openaire   +4 more sources

SDF‐1 Attenuates Oocyte Quality Decline During Reproductive Aging Through Autophagy‐Enhanced Stress Granule Scavenging

open access: yesAdvanced Science, EarlyView.
SDF‐1 levels decline significantly with maternal aging. Exogenous supplementation restores meiotic spindle morphology, chromosomal alignment, and mitochondrial function while reducing oxidative stress in aged oocytes. Mechanistically, SDF‐1 enhances autophagic activity to clear accumulated stress granules, thereby rescuing fertilization competence and ...
Rui Long   +12 more
wiley   +1 more source

CXCR4: from B-cell development to B cell–mediated diseases

open access: yesLife Science Alliance
This review provides an overview of the role of the C-X-C chemokine receptor type 4 (CXCR4) in B-cell development and in B cell–mediated disorders. Chemokine receptors are members of the G protein–coupled receptor superfamily.
Stéphane Giorgiutti   +3 more
doaj   +1 more source

Home - About - Disclaimer - Privacy