CCBP2 Blocking Peptide
- Known as:
- CCBP2 Blocking Peptide
- Catalog number:
- 33r-5612
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CCBP2 Blocking Peptide
Related genes to: CCBP2 Blocking Peptide
- Gene:
- ACKR2 NIH gene
- Name:
- atypical chemokine receptor 2
- Previous symbol:
- CMKBR9, CCBP2
- Synonyms:
- CCR10, D6, CCR9
- Chromosome:
- 3p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2016-10-05
- Gene:
- ACKR4 NIH gene
- Name:
- atypical chemokine receptor 4
- Previous symbol:
- CCRL1
- Synonyms:
- CCR11, CCBP2, VSHK1, CCX-CKR, PPR1
- Chromosome:
- 3q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-18
- Date modifiied:
- 2016-10-05
Related products to: CCBP2 Blocking Peptide
Related articles to: CCBP2 Blocking Peptide
- Breast cancer (BC) remains one of the most prevalent and deadly malignancies among women globally. A deeper understanding of the molecular mechanisms driving BC progression and metastasis is essential for the development of effective therapeutic strategies. While traditional chemokine receptors are well known for their roles in immune cell migration and positioning, atypical chemokine receptors (ACKRs) have recently gained attention as key modulators in cancer-related processes. Unlike conventional receptors, ACKRs-comprising ACKR1, ACKR2, ACKR3, and ACKR4-primarily function by scavenging chemokines, regulating their availability, and modulating receptor signaling in a ligand-independent manner. This review aims to elucidate the roles of ACKRs in BC, focusing on their influence on the tumor microenvironment (TME), cancer cell proliferation, survival, metastasis, and angiogenesis. Additionally, we will explore the potential of ACKRs as diagnostic and prognostic markers and assess their viability as therapeutic targets. By synthesizing recent research findings and highlighting future research directions, this review seeks to provide a comprehensive understanding of the significance of ACKRs in BC and underscore the need for continued investigation into their therapeutic potential. - Source: PubMed
Publication date: 2024/11/11
Yin QinanYang YishaQu ZhifengOuchari MounaZeng LiTang SiyaZheng JiayuZhang ShunshunMa HaodiChen YouyouWang JiayiShi LinlinZheng Xuewei - Acute myeloid leukemia (AML) is a type of leukemia with a very poor prognosis. Consequently, this neoplasm is extensively researched to discover new therapeutic strategies. One area of investigation is the study of intracellular communication and the impact of the bone marrow microenvironment on AML cells, with chemokines being a key focus. The roles of β-chemokines, γ-chemokines, and δ-chemokines in AML processes have not yet been sufficiently characterized. - Source: PubMed
Publication date: 2024/09/24
Korbecki JanBosiacki MateuszStasiak PiotrSnarski EmilianBrodowska AgnieszkaChlubek DariuszBaranowska-Bosiacka Irena - Atypical chemokine receptors (ACKRs) are a group of seven-transmembrane spanning serpentine receptors that are structurally homologous to classical G-protein-coupled receptors and bind cognate chemokines with high affinities but do not signal via G-proteins or mediate cell migration. However, ACKRs efficiently modify the availability and function of chemokines in defined microanatomical environments, can signal via intracellular effectors other than G-proteins, and play complex roles in physiology and disease, including in cancer. In this review, we summarize the findings on the diverse contributions of individual ACKRs to cancer development, progression, and tumor-host interactions. We discuss how changes in ACKR expression within tumor affect cancer growth, tumor vascularization, leukocyte infiltration, and metastasis formation, ultimately resulting in differential disease outcomes. Across many studies, ACKR3 expression was shown to support tumor growth and dissemination, whereas ACKR1, ACKR2, and ACKR4 in tumors were more likely to contribute to tumor suppression. With few notable exceptions, the insights on molecular and cellular mechanisms of ACKRs activities in cancer remain sparse, and the intricacies of their involvement are not fully appreciated. This is particularly true for ACKR1, ACKR2 and ACKR4. A better understanding of how ACKR expression and functions impact cancer should pave the way for their future targeting by new and effective therapies. - Source: PubMed
Publication date: 2024/01/23
Samus MarynaRot Antal - Breast cancer (BC) is by far the most prevalent malignancy found in the female population. Atypical chemokine receptors (ACKRs) are a subclass of G-protein-coupled receptors, which are characterized by disrupted ligand binding and a breakdown of signaling following ligand binding. The evolution and function of multiple ACKRs in BC have yet to be fully elucidated, although certain findings on this family have been reported in several studies in and other species. The present study identified that the expression level of ACKRs was significantly lower in breast carcinoma (BRCA) tissues compared with normal breast tissues through searches of the Tumor Immune Estimation Resource, UALCAN and Gene Expression Profiling Interactive Analysi databases. Additionally, when comparing BRCA tissues with normal breast tissues, it was found that there was obvious hypomethylation in the promoters of and , as well as a marked hypermethylation in the promoters of and In determining the prognosis of patients with BRCA, the expression levels of ACKR1, ACKR2, ACKR3, ACKR4 and ACKR6 were all found to be important factors. The values for distant metastasis-free survival (DMFS), overall survival (OS) and recurrence-free survival (RFS) were all found to be lower in patients with BRCA who had a low expression level of ACKR1. In addition, the RFS rates for patients with BRCA were lower when the expression of ACKR2 was low, and worse values for DMFS, OS and RFS were found to be highly correlated with higher expression levels of ACKR3. Moreover, the DMFS, OS, RFS and predictive power score values were worse in those patients with low ACKR4 expression, and the RFS values for patients with BRCA were also found to be lower when the expression level of ACKR6 was low. Additionally, dendritic cells, macrophages, neutrophils, T cells with CD4 status, T cells with CD8 status and B cells were all substantially linked with ACKR expression, as well as immune cell infiltration. Taken together, the findings of the present study may offer a theoretical foundation for the creation of novel targets and prognostic indicators for BRCA therapy. - Source: PubMed
Publication date: 2023/08/14
Yang LixianZhang ShiyuPu Pengpeng - Atypical chemokine receptors (ACKRs) form a small subfamily of receptors (ACKR1-4) unable to trigger G protein-dependent signaling in response to their ligands. They do, however, play a crucial regulatory role in chemokine biology by capturing, scavenging or transporting chemokines, thereby regulating their availability and signaling through classical chemokine receptors. ACKRs add thus another layer of complexity to the intricate chemokine-receptor interaction network. Recently, targeted approaches and screening programs aiming at reassessing chemokine activity towards ACKRs identified several new pairings such as the dimeric CXCL12 with ACKR1, CXCL2, CXCL10 and CCL26 with ACKR2, the viral broad-spectrum chemokine vCCL2/vMIP-II, a range of opioid peptides and PAMP-12 with ACKR3 as well as CCL20 and CCL22 with ACKR4. Moreover, GPR182 (ACKR5) has been lately proposed as a new promiscuous atypical chemokine receptor with scavenging activity notably towards CXCL9, CXCL10, CXCL12 and CXCL13. Altogether, these findings reveal new degrees of complexity of the chemokine network and expand the panel of ACKR ligands and regulatory functions. In this minireview, we present and discuss these new pairings, their physiological and clinical relevance as well as the opportunities they open for targeting ACKRs in innovative therapeutic strategies. - Source: PubMed
Publication date: 2023/04/20
Szpakowska MartynaD'Uonnolo GiuliaLuís RafaelAlonso Bartolomé AnaThelen MarcusLegler Daniel FChevigné Andy