Anti_Human, mab CXCR1 Source Mouse
- Known as:
- Anti_Human, mab CXCR1 Source Mouse
- Catalog number:
- 101-M360
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CXCR1 Source Mouse
Related genes to: Anti_Human, mab CXCR1 Source Mouse
- Gene:
- CXCR1 NIH gene
- Name:
- C-X-C motif chemokine receptor 1
- Previous symbol:
- CMKAR1, IL8RA
- Synonyms:
- CKR-1, CDw128a, CD181
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-09
- Date modifiied:
- 2016-03-14
- Gene:
- XCR1 NIH gene
- Name:
- X-C motif chemokine receptor 1
- Previous symbol:
- GPR5, CCXCR1
- Synonyms:
- -
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-25
- Date modifiied:
- 2016-10-05
Related products to: Anti_Human, mab CXCR1 Source Mouse
Related articles to: Anti_Human, mab CXCR1 Source Mouse
- : Classical follicular lymphoma (FL) is a heterogeneous malignancy. Early progression within 24 months (POD24) is linked to poor outcomes. However, precise risk stratification remains unclear. We aimed to explore chemokine receptor (CR) expression profiles as potential markers of disease biology and outcome in FL. : We analyzed mRNA expression of , -, , and in 52 FL samples (13 POD24, 39 non-POD24) using RT-qPCR. Immunohistochemistry for CCR3, CCR7, CXCR3, CXCR4, and CXCR5 was performed. Reactive tonsils ( = 5) served as controls. : Compared to controls, FL samples showed lower , , , , , and but higher , , , and expression. Grade 3a FL correlated with reduced , , and , and increased . POD24 cases had elevated , , CCR7, , and but reduced . High , , and levels were linked to inferior survival. Cluster analysis revealed two CR-based subgroups; most POD24 cases clustered in the group with worse prognosis. : These findings suggest distinct chemokine receptor expression profiles contribute to FL progression. Our data highlight several CRs as candidate prognostic markers and potential therapeutic targets in the context of POD24, warranting further investigation in larger, prospective cohorts. : The authors have confirmed clinical trial registration is not needed for this submission. - Source: PubMed
Publication date: 2025/08/28
Zupo AntonellaPansy KatrinGaksch LukasWaldhart JuliaBrunner AndreaStrobl JohannaSzmyra-Polomka MartaHaingartner SandraTomazic Peter VGreinix Hildegard TUhl BarbaraFeichtinger JuliaStary GeorgHaybaeck JohannesVagena Fotini RosiZacharias MartinBeham-Schmid ChristineNeumeister PeterProchazka Katharina TheresaDeutsch Alexander J A - Recently, a strategy involving the engineering of chemokine receptors on immune cells was developed to optimize adoptive cell therapy (ACT) for solid tumors. Given the variability in chemokine secretion among different tumor types, identifying and modulating the appropriate chemokine receptors is crucial. In this study, we utilized extensive RNA sequencing data from both tumor tissues from The Cancer Genome Atlas and normal tissues from Genotype-Tissue Expression to investigate the expression profiles of chemokines. Through analysis, we identified eight chemokine receptors associated with increased chemokine levels in tumor tissues compared to normal tissues, making them promising candidates for enhancing ACT. Subsequent examination of tumor-infiltrating lymphocytes and chimeric antigen receptor-T cells revealed that five out of the eight candidate chemokine receptors did not exhibit elevated expression in T cells. Among five candidates, we demonstrated that CXCR5 is a particularly promising candidate for enhancing cell migration without compromising cell viability or cytotoxicity. In conclusion, our study underscores the potential of five chemokine receptors (CCR6, CCR9, CXCR1, CXCR5, and XCR1) as valuable targets for modulating ACT to enhance cell trafficking and potentially improve cancer therapy outcomes. - Source: PubMed
Publication date: 2025/01/16
Han DoYeonJeong Byung-KwanHong Jong MooSeo Jeong-HanLee GunHeeKim KwangheeHong ChorongLee HyeonjinCha Su MinKim Jong HyeokPark TaehyunGong GyungyubLee Hee Jin - Neuropathic pain is a debilitating condition that affects millions of people worldwide. Numerous studies indicate that this type of pain is a chronic condition with a complex mechanism that tends to worsen over time, leading to a significant deterioration in patients' quality of life and issues like depression, disability, and disturbed sleep. Presently used analgesics are not effective enough in neuropathy treatment and may cause many side effects due to the high doses needed. In recent years, many researchers have pointed to the important role of chemokines not only in the development and maintenance of neuropathy but also in the effectiveness of analgesic drugs. Currently, approximately 50 chemokines are known to act through 20 different seven-transmembrane G-protein-coupled receptors located on the surface of neuronal, glial, and immune cells. Data from recent years clearly indicate that more chemokines than initially thought (CCL1/2/3/5/7/8/9/11, CXCL3/9/10/12/13/14/17; XCL1, CX3CL1) have pronociceptive properties; therefore, blocking their action by using neutralizing antibodies, inhibiting their synthesis, or blocking their receptors brings neuropathic pain relief. Several of them (CCL1/2/3/7/9/XCL1) have been shown to be able to reduce opioid drug effectiveness in neuropathy, and neutralizing antibodies against them can restore morphine and/or buprenorphine analgesia. The latest research provides irrefutable evidence that chemokine receptors are promising targets for pharmacotherapy; chemokine receptor antagonists can relieve pain of different etiologies, and most of them are able to enhance opioid analgesia, for example, the blockade of CCR1 (J113863), CCR2 (RS504393), CCR3 (SB328437), CCR4 (C021), CCR5 (maraviroc/AZD5672/TAK-220), CXCR2 (NVPCXCR220/SB225002), CXCR3 (NBI-74330/AMG487), CXCR4 (AMD3100/AMD3465), and XCR1 (vMIP-II). Recent research has shown that multitarget antagonists of chemokine receptors, such as CCR2/5 (cenicriviroc), CXCR1/2 (reparixin), and CCR2/CCR5/CCR8 (RAP-103), are also very effective painkillers. A multidirectional strategy based on the modulation of neuronal-glial-immune interactions by changing the activity of the chemokine family can significantly improve the quality of life of patients suffering from neuropathic pain. However, members of the chemokine family are still underestimated pharmacological targets for pain treatment. In this article, we review the literature and provide new insights into the role of chemokines and their receptors in neuropathic pain. - Source: PubMed
Publication date: 2023/07/30
Pawlik KatarzynaMika Joanna - Chemokine receptors and their ligands have been identified as playing an important role in the development of diffuse large B-cell lymphoma (DLBCL), follicular lymphoma, and Richter syndrome (RS). Our aim was to investigate the different expression profiles in de novo DLBCL, transformed follicular lymphoma (tFL), and RS. Here, we profiled the mRNA expression levels of 18 chemokine receptors (-, -, and ) using RQ-PCR, as well as immunohistochemistry of seven chemokine receptors (CCR1, CCR4-CCR8 and CXCR2) in RS, de novo DLBCL, and tFL biopsy-derived tissues. Tonsil-derived germinal center B-cells (GC-B) served as non-neoplastic controls. The chemokine receptor expression profiles of de novo DLBCL and tFL substantially differed from those of GC-B, with at least 5-fold higher expression of 15 out of the 18 investigated chemokine receptors (-, , , , , and ) in these lymphoma subtypes. Interestingly, the de novo DLBCL and tFL exhibited at least 22-fold higher expression of , , , and compared with RS, whereas no significant difference in chemokine receptor expression profile was detected when comparing de novo DLBCL with tFL. Furthermore, in de novo DLBCL and tFLs, a high expression of CCR7 was associated with a poor overall survival in our study cohort, as well as in an independent patient cohort. Our data indicate that the chemokine receptor expression profile of RS differs substantially from that of de novo DLBCL and tFL. Thus, these multiple dysregulated chemokine receptors could represent novel clinical markers as diagnostic and prognostic tools. Moreover, this study highlights the relevance of chemokine signaling crosstalk in the tumor microenvironment of aggressive lymphomas. - Source: PubMed
Publication date: 2022/07/17
Uhl BarbaraProchazka Katharina TPansy KatrinWenzl KerstinStrobl JohannaBaumgartner ClaudiaSzmyra Marta MWaha James EWolf AxelTomazic Peter VSteinbauer ElisabethSteinwender MariaFriedl SabineWeniger MarcKüppers RalfPichler MartinGreinix Hildegard TStary GeorgRamsay Alan GApollonio BenedettaFeichtinger JuliaBeham-Schmid ChristineNeumeister PeterDeutsch Alexander J - The focus of this study was to determine which chemokine receptors are present on oral fibroblasts and whether these receptors influence proliferation, migration, and/or the release of wound healing mediators. This information may provide insight into the superior wound healing characteristics of the oral mucosa. The gingiva fibroblasts expressed 12 different chemokine receptors (CCR3, CCR4, CCR6, CCR9, CCR10, CXCR1, CXCR2, CXCR4, CXCR5, CXCR7, CX3CR1, and XCR1), as analyzed by flow cytometry. Fourteen corresponding chemokines (CCL5, CCL15, CCL20, CCL22, CCL25, CCL27, CCL28, CXCL1, CXCL8, CXCL11, CXCL12, CXCL13, CX3CL1, and XCL1) were used to study the activation of these receptors on gingiva fibroblasts. Twelve of these fourteen chemokines stimulated gingiva fibroblast migration (all except for CXCL8 and CXCL12). Five of the chemokines stimulated proliferation (CCL5/CCR3, CCL15/CCR3, CCL22/CCR4, CCL28/CCR3/CCR10, and XCL1/XCR1). Furthermore, CCL28/CCR3/CCR10 and CCL22/CCR4 stimulation increased IL-6 secretion and CCL28/CCR3/CCR10 together with CCL27/CCR10 upregulated HGF secretion. Moreover, TIMP-1 secretion was reduced by CCL15/CCR3. In conclusion, this in-vitro study identifies chemokine receptor-ligand pairs which may be used in future targeted wound healing strategies. In particular, we identified the chemokine receptors CCR3 and CCR4, and the mucosa specific chemokine CCL28, as having an predominant role in oral wound healing by increasing human gingiva fibroblast proliferation, migration, and the secretion of IL-6 and HGF and reducing the secretion of TIMP-1. - Source: PubMed
Publication date: 2017/05/23
Buskermolen Jeroen KRoffel SanneGibbs Susan