Polyclonal Rabbit CXCR7 Antibody
- Known as:
- Polyclonal Rabbit CXCR7 Antibody
- Catalog number:
- KA0941
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit CXCR7 Antibody
Related genes to: Polyclonal Rabbit CXCR7 Antibody
- Gene:
- ACKR3 NIH gene
- Name:
- atypical chemokine receptor 3
- Previous symbol:
- CMKOR1, CXCR7
- Synonyms:
- RDC1, GPR159
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-01
- Date modifiied:
- 2014-11-19
Related products to: Polyclonal Rabbit CXCR7 Antibody
Related articles to: Polyclonal Rabbit CXCR7 Antibody
- Airflow obstruction unresponsive to β2 adrenergic receptor (β2AR) agonists is a key feature of infant respiratory syncytial virus (RSV) bronchiolitis. The underlying mechanisms remain poorly understood, and effective treatment is lacking. - Source: PubMed
Publication date: 2026/02/24
Zhao CaiqiTaliento Alice EBelkin Elise MFearns RachelLerou Paul HAi XingbinBai Yan - Arrestins regulate G protein-coupled receptor (GPCR) signaling by binding phosphorylated receptors embedded in lipid bilayers, yet how receptor phosphorylation and membrane composition cooperate to control arrestin activation remains unclear. Here, we reconstitute this interplay using N-terminally palmitoylated phosphopeptides tethered to nanodiscs of defined lipid composition and quantitatively measure arrestin-2 (Arr2) activation and membrane engagement. We find that both receptor phosphorylation and the lipid environment are essential for robust Arr2 activation, with phosphoinositides (PIPs) and other anionic lipids facilitating Arr2 activation and membrane association through distinct mechanisms. Systematic profiling of phosphorylation barcodes derived from atypical chemokine receptor 3 (ACKR3) and vasopressin receptor 2 (VR) identifies phospho-motifs that potently activate Arr2. Moreover, the position of these motifs relative to the membrane determines Arr2 engagement, supporting a model of regional phosphorylation barcodes. Genome-wide motif analysis further links the phosphorylation barcode to predicted arrestin coupling strength and classification into Class A or Class B GPCRs. Finally, lipidated phosphopeptides inhibit GPCR-Arr2 interactions in live cells and enable structural characterization of Arr2-phosphopeptide complexes by cryo-electron microscopy, establishing a membrane-integrated framework for decoding arrestin response. - Source: PubMed
Publication date: 2026/04/17
Aydin YasminZhuo YaYen Yu-ChenChen Chun-LiangKlug Candice SMarchese AdrianoChen Qiuyan - - Source: PubMed
Publication date: 2026/04/23
Kuppens AmandineRogister BernardNeirinckx Virginie - Airborne polycyclic aromatic hydrocarbons (PAHs) are increasingly linked to asthma onset and exacerbation, yet their molecular mechanisms remain unclear. Building on our previous finding that PM2.5 alters m6A RNA methylation, we hypothesized that PAHs drive asthma progression through epitranscriptomic regulation. Here, we show that PAH exposure aggravated lung injury, airway remodeling, and fibrosis while reducing global m6A levelsan effect reversed by AhR inhibition. Mechanistically, PAH-activated AhR suppressed transcription of the m6A demethylase FTO, leading to widespread hypomethylation. Reduced m6A deposition on ACKR3 mRNA enhanced its stability through IGF2BP1/2/3 binding, thereby increasing ACKR3 expression. Elevated ACKR3 promoted autophagy and inflammatory signaling in bronchial epithelial cells. Consistently, FTO-deficient mice displayed exacerbated airway inflammation, fibrosis, and ACKR3-driven autophagy. Moreover, PAHs activated the TNFα/NF-κB pathway, further amplifying autophagy and inflammation. Together, these findings define a previously unrecognized AhR-FTO-ACKR3 epitranscriptomic axis through which PAHs potentiate NF-κB signaling, autophagy, and airway injury, providing new mechanistic insight and potential therapeutic targets for pollution-driven asthma. - Source: PubMed
Publication date: 2025/11/04
Liu ShengbinChu JiangzhouXin JinxiuYin XiaolinHe ZhongshanQin ShugangSong Xiangrong - Congenital cranial dysinnervation disorders (CCDDs) are a group of rare, nonprogressive conditions characterized by abnormal development of the cranial motor nerves and variable ocular motility deficits, ptosis, incomitant strabismus, and facial palsy. Advances in genetics and neuroimaging have revealed that these disorders result from defects in neuronal differentiation or axon guidance of the cranial motor neurons. Duane retraction syndrome, the most common CCDD, results from the absence of the abducens nerve and innervation of the lateral rectus by oculomotor nerve axons; causative genes include CHN1, MAFB, HOXA1, SALL4, and EBF3, although most cases do not have a genetic diagnosis. Congenital fibrosis of the extraocular muscles (CFEOM), results from variants in KIF21A, PHOX2A, TUBB3, or other tubulin genes, and affects the oculomotor and trochlear nerves. Horizontal gaze palsy with progressive scoliosis (HGPPS), caused by ROBO3 loss of function, arises from failure of axonal midline crossing in the brainstem. Moebius syndrome, defined by abducens and facial nerve palsies, has no identified genetic cause and may result from non-Mendelian causes. Additional CCDDs with atypical or syndromic presentations are linked to COL25A1, ECEL1, and ACKR3, although many do not have a genetic explanation. The expanding list of CCDD-associated genes highlights shared developmental pathways, including neuronal differentiation, axon guidance, and microtubule dynamics. Improved genetic diagnosis informs prognosis and multidisciplinary management. This review synthesizes current understanding of CCDDs, emphasizing the shift from phenotypic classification to molecular subtyping, and underscores the importance of ongoing research to resolve genetically unsolved cases and refine diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/03/23
Aufderheide KathleenWhitman Mary C