CCR5 (N-Terminus) Peptide
- Known as:
- CCR5 (N-Terminus) Peptide
- Catalog number:
- 1112P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CCR5 (N-Terminus) Peptide
Related genes to: CCR5 (N-Terminus) Peptide
- Gene:
- CCR5 NIH gene
- Name:
- C-C motif chemokine receptor 5 (gene/pseudogene)
- Previous symbol:
- CMKBR5
- Synonyms:
- CKR-5, CC-CKR-5, CKR5, CD195, IDDM22
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1996-05-15
- Date modifiied:
- 2019-01-10
Related products to: CCR5 (N-Terminus) Peptide
Related articles to: CCR5 (N-Terminus) Peptide
- Post-translational sulfation of the chemokine receptor CCR5 is involved in crucial biological processes such as viral infection and chemokine signaling. This sulfation can occur at the N-terminal tyrosine residues (Y3, Y10, Y14, and Y15) of CCR5 and is catalyzed by human tyrosylprotein sulfotransferases (hTPSTs) within the Golgi lumen. However, the detailed molecular mechanism by which these tyrosine residues are sulfated remains unresolved. To elucidate the mechanism, we determined the crystal structure of a soluble domain of hTPST1 bound to the sulfate donor product 3'-phosphoadenosine 5'-phosphate (PAP) and a modified 18-residue CCR5 peptide designed to isolate the Y3-centered binding mode, at 3.2 Å resolution, with six peptide residues ordered. This structure defines key interactions consistent with Y3 sulfation and is consistent with previous biochemical data. Based on the crystal structure and prior knowledge, we constructed peptide docking models for Y10, Y14, and Y15 sulfation, as well as full-length hTPST1-PAP-CCR5 docking models. The crystal structure provides experimental insight into Y3 recognition, whereas the docking models provide testable hypotheses for how the other sulfation sites may be accommodated in the context of CCR5. - Source: PubMed
Publication date: 2026/05/22
Tanaka ShinnosukeAsano HiraiToyoda KotaNishiyori ToshiakiKojo HidetakaKiyomatsu KazutoKurogi KatsuhisaSakakibara YoichiNishimoto EtsukoTeramoto TakamasaKakuta Yoshimitsu - Head and neck adenoid cystic carcinoma (HNACC) is an uncommon but aggressive salivary gland malignancy with high recurrence and metastasis rates. Its "immune-cold" phenotype limits the efficacy of systemic therapy, and thus, radiotherapy is the principal treatment for unresectable cases. However, frequent radioresistance suggests the involvement of distinct molecular drivers. This study investigated the role of CCL5 in HNACC radioresistance, its mechanistic link to autophagy, and its potential as a radiosensitization target. - Source: PubMed
Publication date: 2026/05/20
Tan MingyuChen YanliangYang JinxinWang QianLi Lu - Subarachnoid hemorrhage (SAH) triggers robust neuroinflammatory responses that contribute to secondary brain injury, with microglia acting as central mediators; however, the upstream regulators governing microglial activation remain incompletely understood. To address this, we investigated the role of C-C chemokine receptor 5 (CCR5) using a murine endovascular perforation SAH model. Expression profiling revealed that CCR5 is rapidly upregulated after SAH, with prominent expression in microglia in the cortex and perilesional region. We then evaluated the therapeutic efficacy of pharmacological inhibition using the intranasal CCR5 antagonist maraviroc (MVC). MVC treatment successfully shifted microglia toward an anti-inflammatory phenotype and reduced pro-inflammatory cytokines. This inflammatory modulation attenuated brain edema, suppressed neuronal apoptosis, and significantly improved both early and long-term neurological outcomes. Furthermore, in vitro experiments confirmed that MVC reverses oxyhemoglobin-induced pro-inflammatory microglial polarization, indirectly protecting neurons from microglia-dependent injury. Collectively, these findings identify CCR5 as an important regulator of microglia-associated neuroinflammation after SAH and suggest that MVC exerts neuroprotection, at least in part, through modulation of the CCR5-related inflammatory microenvironment. - Source: PubMed
Publication date: 2026/05/20
Ye JiasenLi HangyangPeng ZhenghongDuan ZuoyueChen QiangJiang YongTu TianqiPeng Jianhua - Chronic hepatitis B (CHB) caused by the hepatitis B virus (HBV) remains a major global health burden. The immune-active (IA) phase, characterized by positive Hepatitis B surface antigens (HBsAg), elevated alanine transaminase (ALT) levels, and detectable HBV DNA, is a pivotal period in the natural history of CHB. Understanding the biological process in this phase is critical for elucidating CHB pathogenesis. With the accumulation of multi-omics data, it has become feasible to identify key molecular targets regulating the host-virus interaction during the IA phase. Identifing these targets provides a critical foundation for developing novel strategies to modulate the host immune response as an important supplement to antiviral therapy. - Source: PubMed
Publication date: 2026/05/04
Li FangfangLi YiDu YirongFan ChaoXiong JunHu FeiDeng XiaoyingWang XiaoyanShi HongyanSun XiangweiZheng XuyangZhang Ying - Doxorubicin (Dox)-induced cardiotoxicity (DIC) remains a challenge in tumor chemotherapy. Targeting macrophage-secreted molecules is a potential strategy to mitigate DIC. Transcriptome analysis of RAW264.7 cells treated with 100 nM Dox revealed increases in 33 proteins located in the extracellular space, including CCL5. An animal model of DIC characterized by degree I atrioventricular block was established in 9-12 weeks old male C57BL/6 mice through three doses of 5 mg/kg Dox intraperitoneally (i.p.) administered every third day. The plasma CCL5 level in these mice consistently increased, which could be attenuated by macrophage depletion using clodronate liposome (15 mg/kg, i. p.). In pharmacological experiments with these animals, administration of maraviroc (MVC) (50 mg/kg, i. p., daily) prevented PR interval elongation caused by Dox. Both in vitro and in vivo experiments showed that MVC attenuated Ca overload induced by CCL5 in H9C2 cells and by Dox in cardiomyocytes from DIC models. Further in vitro experiments confirmed that CCL5 decreases the SERCA2a level and PKA-C, PLB phosphorylation in H9C2 cells, exacerbating Ca overload and CaMKII phosphorylation, which can be attenuated by MVC administration. In conclusion, Dox can induce an increase in macrophage-derived CCL5 in plasma, and MVC targeting the CCL5's receptor CCR5 can ameliorate atrioventricular block caused by Dox toxicity, suggesting that it may be a candidate for DIC treatment in chemotherapy. - Source: PubMed
Publication date: 2026/05/18
Wang HengZhang YuShen LiWu GangningYu HengZhang LuzhengSun YujinXue Song