CCM2 Over-expression Lysate Product
- Known as:
- CCM2 Over-expression Lysate Product
- Catalog number:
- GWB-EFF96A
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- CCM2 Over-expression Lysate Product
Related genes to: CCM2 Over-expression Lysate Product
- 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 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: CCM2 Over-expression Lysate Product
- 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 - Actin cytoskeleton dysregulation contributes to vascular anomalies such as cerebral cavernous malformation (CCM). Talin rod domain containing-1 (TLNRD1) has been reported to interact with cerebral cavernous malformations 2 protein (CCM2), yet the downstream signaling remains debated, as previous studies have described opposite directions of Krueppel-like factor 2/4 (KLF2/4) changes after TLNRD1 depletion. Here, we combined biochemical analyses, structural modeling, transcriptomics, and single-cell network perturbation to examine the TLNRD1-CCM2 axis in endothelial cells. Coimmunoprecipitation and mass spectrometry confirmed the association between TLNRD1 and the CCM complex. Furthermore, protein docking predicted a stable TLNRD1-CCM2 interface (ΔG ≈ -50.36 kcal/mol) supported by prominent hydrogen bonds. Bulk RNA sequencing following TLNRD1 knockdown identified 677 differentially expressed genes, which were heavily enriched for actin cytoskeleton organization, with limited support for activation of the canonical MEKK3-KLF2/4 program. To assess KLF2/4 more directly, we analyzed human CCM single-cell RNA sequencing using scTenifoldKnk alongside complementary in vitro perturbations. Across these orthogonal analyses, KLF2 and KLF4 showed little to no consistent transcriptional alterations. Instead, TLNRD1 perturbation prominently altered endothelial F-actin stress fiber formation. Together, these data support a model in which TLNRD1 preferentially modulates endothelial cytoskeletal remodeling largely independent of overt KLF2/4 transcriptional shifts, helping to contextualize previous discrepancies and refining our understanding of its role in vascular biology. - Source: PubMed
Publication date: 2026/06/01
Zhang YuchongQiu ShoujiHu ChengkaiFu WeiguoWang ChenjiWang Lixin - Recently, high-endurance ferroelectric HfO is highly desirable since the emerging of in-memory computing requires non-volatile memories not only to store data but also to execute computation, challenging writing/erasure switching reliability. Understanding and exploitation of the polarization fatigue diagram are crucial for improving endurance performances. Here, we show fatigue-resistant Sm:HfO thin films by modulating grain boundaries (GBs) in orientation-controllable orthorhombic phase. On GBs, orientation discontinuity raises energy levels of O 2p orbitals due to lattice distortion, which promote electron accumulation and yield a high-symmetry structural transform at the boundary, facilitating 90° switching of out-of-plane domains because of lowered switching barrier. Then the domains are frozen in plane by the charged GBs and polarization fatigue takes place. By eliminating GBs associated with phase transform, remarkably-improved fatigue resistance is achieved in uniform 180° switching, which exhibits the increase of fatigue-free endurance by 200 times to 2.0 × 10 cycles with, more importantly, a large field-cycling non-volatile polarization of ∼60 µC/cm, showing the state-of-the-art endurance performances in hafnium oxides. Roadmaps of the fatigue scenarios are given based on key roles of GBs in domain configurations and switching pathways. Our findings open a new perspective for fatigue studying and guide the material design of high-reliability hafnium oxide memories. - Source: PubMed
Publication date: 2026/07/03
Li JiufuLin ZehaoJing XixiangZheng WeijieWang ZhenJiang XinyuXu JiboZheng ChunyanLiu XiaohuiFu BeibeiHuang HaoliangWang Huan-HuaWu DiSong KepengCao TengfeiWen Zheng