Ramp1 (C_Term., mouse)
- Known as:
- Ramp1 (C_Term., mouse)
- Catalog number:
- Y214171
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Ramp1 (C_Term. mouse)
Related genes to: Ramp1 (C_Term., mouse)
- Gene:
- RAMP1 NIH gene
- Name:
- receptor activity modifying protein 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2017-12-06
Related products to: Ramp1 (C_Term., mouse)
Related articles to: Ramp1 (C_Term., mouse)
- Breast cancer is globally the most common cancer among women. Although the five-year survival rate exceeds 80% for patients with localized disease, it drops to approximately 30% once metastasis occurs, underscoring the urgent need to define mechanisms that drive metastatic progression. Breast is a highly innervated organ and most of its innervation is sensory. However, whether sensory neurons can directly impact breast cancer cells remains an understudied topic. Here, we show that mammary tumors have increased CGRP⁺ sensory innervation. Using our novel microfluidic Device for Cancer cell-Axon Interaction Testing (DACIT), we demonstrate that the presence of axons strongly inhibits ECM-degrading ability of cancer cells. The sensory neuron secretome suppresses assembly and function of invadopodia, which are cancer cell protrusions controlling ECM degradation, and essential for intravasation and metastasis. We identify calcitonin gene-related peptide (CGRP) as the key component of the sensory neuron secretome responsible for the inhibitory effect. CGRP signaling occurs through the CRLR/RAMP1 receptor complex expressed by breast cancer cells, inducing a rapid increase in intracellular cAMP levels in breast cancer cells, followed by an increase in RhoC activity and suppression of invadopodia and ECM degradation. Loss of RAMP1 function enhances 3D spheroid invasion, cancer cell motility and significantly increases the number and the size of lung metastatic foci. Consistently, analyses of both mouse and human RNASeq data point to a link between increasingly invasive subtypes with a gradual decrease in expression of RAMP1 and CRLR. To validate findings, we compare RAMP1 expression in the patient breast tumors with adjacent normal tissues, confirming the invasive breast tumors have reduced levels of RAMP1. Together, our findings identify a protective role for the paracrine CGRP signaling in limiting breast cancer invasion and metastasis. We also demonstrate how cancer cells circumvent CGRP inhibition by suppressing RAMP1 expression, highlighting CGRP-RAMP1-cAMP axis as a potential therapeutic target in breast cancer. - Source: PubMed
Publication date: 2026/04/21
Velazquez-Quesada InesBelova ElizavetaJarrah AfroozMariano Maria Carolina CesarDahleh Yasminede Assis Lima MaíraCosta Debora Barbosa VendraminiFrancescone RalphCukierman EdnaHodgson LouisGligorijevic Bojana - Innervation propels tumor progression through intricate mechanisms. Recently, Zhang et al. demonstrated that sensory neurons interact with cancer-associated fibroblasts via the calcitonin gene-related peptide (CGRP)-receptor activity-modifying protein 1 (RAMP1) axis to mediate immune exclusion in triple-negative breast cancer. Halting the neuron-fibroblast crosstalk via rimegepant holds promise for reorganizing the extracellular matrix and synergizing with cancer immunotherapy. - Source: PubMed
Publication date: 2026/04/30
Fan PinchaoZhi XiaofeiLiu Weici Laurence - - Source: PubMed
Publication date: 2026/04/21
da Costa Cabral GabrielleRodrigues Letícia Almeidade Almeida Cabral Candiago JúliaProcópio João Felipe Fernandes FerreiraSilva Júlia Costa Cerqueirade Lima Maria Eduarda BarbosaGisela Ellery Costa Lima Ana Stellada Costa Júnior José Valmir Falcãode Araújo David Abner Santosda Silva João Paulo Emilianode Almeida Oliveira Sofia Amanciode Oliveira Calaça Farias Rafaelde Almeida Leonardo Prudêncio Coutinhode Melo Salomão Belfort SparapanXavier José Emersonde Araújo Sandra Taveirosde França-Júnior Raimundo RodriguesDos Santos Lemos Gurgel Maria Améliade Carvalho Fraga Carlos Alberto - Low back pain is a global health problem. Discogenic low back pain, the most common type of low back pain, is closely related to cartilage endplate (CEP) degeneration and inflammation. In this study, by constructing a rat model of lumbar spine instability (LSI) and combining biomechanical analysis with molecular biology techniques, we revealed the central role of the mechanosensitive channel Piezo2 in the vicious cycle of discogenic low back pain. The results revealed that abnormal mechanical stress triggers calcium influx and promotes CGRP release by activating Piezo2 in the dorsal root ganglion (DRG). CGRP synergizes with mechanical force to activate the IKKβ/NF-κB pathway in CEP cells via the receptor RAMP1, which induces the secretion of IL-6 and IL-1β, and further sensitizes DRG neurons, forming a positive feedback loop. Macrophage depletion did not alleviate pain/inflammation. Targeted inhibition of Piezo2 (with AAV-shPiezo2 gene silencing or omega-3 fatty acids) or blockade of CGRP signaling (with Rimegepant) significantly alleviated pain-related behaviors, suppressed inflammation, and delayed CEP degeneration. This study elucidated a novel mechanism by which mechanical‒neuroinflammatory interactions drive the progression of discogenic low back pain and provided a theoretical basis for the development of multitargeted combination treatment strategies. - Source: PubMed
Publication date: 2026/04/16
Xu HanpengGeng WenDu ZhiDu YifanWu DiTong BideLiang HuaizhenZhou XingyuOu ZixuanWei JunyuWang KunSong YuHua WenbinXu YanKe WencanWang BingjinYang Cao - Peptides are desirable therapeutics due to their inherent potency, safety, and ability to engage complex protein surfaces. Slower kinetics of protein-peptide (un)binding can directly influence their drug efficacy and duration of action, in part by improving plasma stability of the peptide. A better understanding of peptide binding mechanisms would benefit for the development of next-generation peptide-based drugs with optimized kinetic properties. The calcitonin receptor-like receptor:receptor activity-modifying proteins 1 (CLR:RAMP1) complex and its endogenous agonist peptide calcitonin gene-related peptide (CGRP) are of particular interest due to their central role in migraine pathophysiology. In this study, we comparatively analyze C-terminal constructs of native CGRP and "ssCGRP," an engineered variant with 430-fold longer residence time in the CLR:RAMP1 complex. Using our high-dimensional weighted-ensemble algorithm, we thoroughly sampled unbinding pathway ensembles for the two peptides. This elucidates the basis of the engineered residence time enhancement for ssCGRP and provides a detailed view of the intra- and intermolecular stabilizing interactions for both peptides in the bound ensemble and along the unbinding transition pathway. The natural dynamics used in weighted ensemble, combined with Markov state modeling, allows for the first comparative analysis of protein-peptide unbinding transition state ensembles between a native and mutant peptide. We find that ssCGRP(27-37) demonstrates enhanced ligand recapture of intermediate unbinding conformations and samples a more heterogeneous bound-state ensemble that entropically stabilizes the bound basin. This study shows the molecular determinants of the residence time of peptides in CLR:RAMP1 and provides valuable insight for the design of long-acting peptide therapeutics. - Source: PubMed
Publication date: 2026/03/09
Kilinc CerenBabin Katie MPioszak Augen ADickson Alex