CCM2 Antibody
- Known as:
- CCM2 Antibody
- Catalog number:
- AF1210a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CCM2 Antibody
Related genes to: CCM2 Antibody
- Gene:
- CCM2 NIH gene
- Name:
- CCM2 scaffold protein
- Previous symbol:
- C7orf22
- Synonyms:
- MGC4607, OSM
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-14
- Date modifiied:
- 2019-04-23
Related products to: CCM2 Antibody
Related articles to: CCM2 Antibody
- Cerebral cavernous malformation (CCM) is a genetic vascular disorder arising from endothelial dysfunction, affecting the microvasculature of the central nervous system. Patients with mutations in any of three genes may suffer from neurological deficits and even hemorrhagic stroke. The three CCM proteins are structurally unrelated and assemble into the CCM complex that forms scaffolds associated with junctional complexes and the actomyosin cytoskeleton. Recent work points to a dual role of the CCM complex in structural scaffolding and mechanosensitive signal transduction. In this review, we highlight recent advances examining the CCM complex's role in organizing various multi-protein interactions and facilitating mechanosensitive signaling that regulates endothelial cell behavior. Importantly, accumulating evidence emphasizes the impact of hemodynamic forces on CCM signaling, pointing to distinct mechanisms in arterial versus venous vessels. Surprisingly, the loss of CCM proteins has vasoprotective effects in arteries but pathological effects in veins and small capillaries. Understanding CCM scaffolds that integrate structural support with mechanosensitive signaling is fundamental to deciphering the molecular mechanisms that underlie physiological versus pathological outcomes within the vasculature. This knowledge advances the development of targeted therapeutic strategies aimed at restoring endothelial integrity and normal vascular function, particularly by modulating signaling pathways influenced by hemodynamic forces. - Source: PubMed
Publication date: 2026/02/25
Rödel Claudia JasminAbdelilah-Seyfried Salim - The rising demand for sustainable packaging materials has driven the use of agro-waste-derived bio-fillers to enhance the functional properties of biodegradable polymers. The aim of this study is to extract cellulose from Pandanus fascicularis Lam fibers (PFLC) and assess its effectiveness as a reinforcing bio-filler in polylactic acid (PLA) biofilms for eco-friendly packaging uses. This study was carried out by isolating Cellulose from PFL fibers via sequential bleaching and acid hydrolysis. PLA biofilms containing 0.5, 1.0, 1.5, 2.0, 2.5, and 3.0 wt% PFLC were fabricated using solution casting techniques. The films were characterized using FTIR, XRD, SEM-EDX, TGA, DSC, mechanical tests, oxygen transmission rate (OTR), water vapor transmission rate (WVTR), contact angle, water absorption, soil biodegradation, and UL-94 flammability tests. The results show that the incorporation of PFLC significantly influenced the performance of PLA films. Tensile strength (22.27 MPa) and Young's modulus (11.31 MPa) improved at 1 wt% PFLC, indicating better interfacial interaction, while higher loadings increased ductility. The lowest OTR of 466 cc/m·day·atm at 2 wt% PFLC, and the lowest WVTR of 84 g/m·day at 2.5 wt% PFLC shows improved barrier properties. Contact angle tests indicated increased hydrophilicity with higher PFLC content. Soil burial tests showed enhanced biodegradation (~48.6% weight loss at 3 wt% after 4 months), and UL-94 testing showed moderate self-extinguishing behavior (V-2 rating). The findings show that 1-2.5 wt% PFLC offers an optimal balance of mechanical, barrier, thermal, and biodegradation properties, highlighting its potential for sustainable packaging applications. - Source: PubMed
Publication date: 2026/08/03
Singh Benny Sharon BlessedGeorge Antony MiraculasThangaraj Gerald Arul Selvan MartinRahel Bella George - Cerebral cavernous malformations (CCMs) are vascular lesions caused by the loss-of-function mutations in one of three CCM genes, CCM1 (KRIT1), CCM2, and CCM3 (PDCD10), or gain-of-function mutation in MAP3K3, which encodes MEKK3. Loss of function in CCM genes leads to pathological activation of MEKK3 signaling. Genetic reduction of MAP3K3 gene dosage or pharmacological inhibition of MEKK3 suppresses CCM formation in mouse models, establishing MEKK3 as a promising therapeutic target for CCM. - Source: PubMed
Publication date: 2026/07/28
Zhao QianqianZheng MinWan XiaoboLi BingjieYang XiGao CaixiaHan ZhimingSun HuabingFu YuanZheng Xiangjian - Familial cerebral cavernous malformation (FCCM) is a hereditary vascular disorder associated with pathogenic variants of , and . Among these, -related FCCM is considered the most severe subtype and is characterized by early onset, multiple lesions, frequent brainstem involvement, and an increased risk of intracranial hemorrhage. Brainstem symptoms may be the initial manifestations. However, isolated oculomotor nerve palsy in childhood is rare. We report the case of a 17-month-old girl with normal developmental milestones who developed mild right ptosis, strabismus, and impaired adduction and upward gaze of the right eye at nine months of age. There was no family history of seizures or intracranial hemorrhage. Computed tomography of the head revealed multiple intracranial calcifications. Susceptibility-weighted angiography (SWAN) magnetic resonance imaging (MRI) revealed multiple cerebral cavernous malformations (CCMs), and follow-up MRI one year later demonstrated new lesions, including pontine involvement. Fast imaging employing steady-state acquisition (FIESTA) revealed hemorrhagic changes adjacent to the right oculomotor nerve within the interpeduncular cistern, suggesting that the partial oculomotor nerve palsy was associated with focal hemorrhagic involvement. Genetic analysis revealed the presence of a novel variant. This case highlights that -related FCCM may initially present with isolated cranial neuropathy during childhood and subsequently show rapid radiological progression. Careful longitudinal follow-up is required because of the risk of future neurological deterioration. - Source: PubMed
Publication date: 2026/06/22
Murakami YoshimiInoue TakanobuIshikura ShunFujimoto RyoAoyama Hiromi - Cerebral cavernous malformations (CCMs) are vascular anomalies prone to hemorrhage, leading to neurological deficits and reduced quality of life. Current therapies are limited, and molecular mechanisms underlying vascular instability remain incompletely understood. MicroRNAs have emerged as key regulators of vascular integrity. This study investigates the role of microRNA-21-3p (miR-21-3p) in modulating oxidative stress and angiogenesis in CCM. - Source: PubMed
Publication date: 2026/07/20
Guo Xin-XingHuang Zhong-RunChen Pei-ShengLi QiLi JiaShi Zhong-Song