Hamster Anti-Mouse CD195
- Known as:
- Hamster Antibody toMouse CD195
- Catalog number:
- 129-10112
- Product Quantity:
- 250
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Hamster Anti-Mouse CD195
Related genes to: Hamster Anti-Mouse CD195
- 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: Hamster Anti-Mouse CD195
Related articles to: Hamster Anti-Mouse CD195
- - Source: PubMed
Publication date: 2026/10/01
Belew Ashton TreyMeskauskas ArturasMusalgaonkar SharmishthaAdvani Vivek MSulima Sergey OKasprzak Wojciech KShapiro Bruce ADinman Jonathan D - Ischemic stroke induces neuronal pyroptosis driven by excessive endoplasmic reticulum (ER) stress, which exacerbates secondary brain injury. Notoginsenoside R1 (NGR1) has demonstrated neuroprotective properties; however, whether its mechanism involves the modulation of chemokine-like factor 1 (CKLF1)-mediated ER stress remains unclear. - Source: PubMed
Publication date: 2026/09/23
Wang HanlongSun YangLiu ShashaChen ChenLong JunpengYan QianLin YutingLi ShuqinHuang YantingLiu FangYang SongweiLin MeiyuLiu XuanYi FanTan YongChen NaihongYang YantaoAi Qidi - Human pregnancy presents a unique physiological state that allows for growth of an antigenically dissimilar foetus. The immune system plays a key role in establishing and maintaining successful pregnancy, yet detailed understanding of immunological responses in pregnancy is lacking. - Source: PubMed
Publication date: 2026/10/01
Habel Jennifer RNguyen Thi H OAllen Lilith FSkinner Morgan JKedzierski LukaszAllen E KaitlynnLi Shihande Alwis NatashaHagen Ruth RDoggett KarenJia XiaoxiaoTarasova IlariyaMinervina Anastasia APogorelyy Mikhail VHolloway Ashleigh IMathew Nikita LSaunders Philippa MClatch AllisonEvrard MaximilienXu CalvinKoay Hui-FernAbdullah-Al-Kamran Khan MdMackay Laura KBarrow Alexander DDouros CeliaKarapanagiotidis TheoNicholson SuellenBond KatherineWilliamson Deborah AHui LisaLappas MarthaWalker SusanNicholson Sandra EHannan Natalie JBrooks Andrew GSchroeder JanCrawford Jeremy ChaseThomas Paul GRowntree Louise CKedzierska Katherine - Ischemic stroke triggers devastating neuronal injury cascades, and ferroptosis acts as a key mediator of post-ischemic neuronal loss. Although C-C chemokine receptor type 5 (CCR5) has been traditionally implicated in post-stroke neuroinflammation, its cell-specific role in neuronal ferroptosis remains obscure. Here, we combined single-cell transcriptomic analysis, a permanent middle cerebral artery occlusion (pMCAO) mouse model, and in vitro hypoxia-ischemia-mimicking conditions to define an endogenous neuroprotective role for neuronal CCR5. Single-cell RNA sequencing revealed a marked upregulation of the CCL-CCR signaling pathway, with CCR5 identified as a prominent hub mediating intercellular interactions. In vivo, CCR5 was significantly elevated in peri-infarct neurons from 48 h up to one month after pMCAO, rather than microglia or astrocytes, suggesting an intrinsic stress response. In vitro, hypoxia-ischemia-mimicking conditions in SH-SY5Y cells and primary cortical neurons recapitulated this compensatory yet insufficient CCR5 induction alongside HIF-1α upregulation, GPX4 depletion, and severe lipid peroxidation. Functional studies demonstrated that CCR5 knockdown or pharmacological inhibition with maraviroc (MVC) further aggravated GPX4 reduction and lipid peroxide accumulation, whereas CCR5 overexpression substantially restored anti-ferroptotic capacity. CCR5 positively regulated AMPK and ACC phosphorylation, and inhibition of AMPK completely abolished CCR5-mediated GPX4 preservation and anti-ferroptotic defense. In vivo, MVC administration further accelerated peri-infarct iron deposition, reduced neuronal survival, and significantly worsened long-term motor deficits in pMCAO mice. Collectively, these findings identify a previously unrecognized endogenous adaptive mechanism whereby ischemia-induced neuronal CCR5 limits ferroptosis through AMPK/ACC-mediated GPX4 maintenance, providing a novel therapeutic conceptualization for strengthening endogenous protective cues in ischemic stroke. - Source: PubMed
Publication date: 2026/09/30
Huang MinhuangWu QilongXie KefanDong ZejinGe YijunLuo XiaoyangFan WentaoChen YuanPing Suning - Ischemic stroke (IS) triggers neuroinflammation cascades where microglial polarization is a pathological determinant. Mailuoning oral liquid (MLN O) is clinically utilized to prevent thrombosis and treat convalescent IS, but its pharmacological targets in permanent IS remain unclear. - Source: PubMed
Publication date: 2026/09/30
Liu XiaoqiongLin YandanLi JianJiang HongSui YihangLi YueyuanFan LinglingChen HaiTan Ninghua