CDH5 antibody - N-terminal region (OAAB01399)
- Known as:
- CDH5 (anti-) - N-terminal region (OAAB01399)
- Catalog number:
- oaab01399
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CDH5 antibody - N-terminal region (OAAB01399)
Related genes to: CDH5 antibody - N-terminal region (OAAB01399)
- Gene:
- CDH5 NIH gene
- Name:
- cadherin 5
- Previous symbol:
- -
- Synonyms:
- 7B4, CD144
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-20
- Date modifiied:
- 2016-10-05
Related products to: CDH5 antibody - N-terminal region (OAAB01399)
Related articles to: CDH5 antibody - N-terminal region (OAAB01399)
- Germline deletion of the core circadian transcription factor Bmal1 has been shown to reduce blood-spinal cord barrier (BSCB) disruption and tissue loss following moderate T9 contusive spinal cord injury (SCI) in mice. Therefore, effects of conditional Bmal1 deletions were tested using the same model. A strong reduction of Bmal1 expression in the brain or spinal cord followed tamoxifen treatment of Bmal1 young adult mice who carried the broadly expressed Cag-CreERT2 recombinase transgene. Supporting functional consequences of such a deficit, canonical BMAL1 target genes Nr1d1 and Dbp were also downregulated. However, only few tissue damage markers were moderately reduced at 3 days post SCI. Furthermore, neither locomotor recovery nor long-term white matter sparing was improved. Similar SCI phenotype was observed in endothelia-selective Bmal1 mice (Cdh5-Cre:Bmal1) including modest attenuation of few acute injury markers, but no significant effects on functional recovery or long-term tissue sparing. These data suggest that germline deletion of Bmal1 is protective against SCI due to compensatory changes in gene expression that originate during development and involve cells beyond endothelia. Therefore, a direct role for BMAL1 in secondary injury cascades that are activated after SCI is unlikely. - Source: PubMed
Publication date: 2026/08/11
Slomnicki Lukasz PArmstrong Christine DMorehouse Johnny RAndres KarienaMusiek Erik SOhri Sujata SaraswatHetman Michal - Severe COVID-19 is frequently associated with vascular complications, raising ongoing debate about whether SARS-CoV-2 can directly infect endothelial cells and thereby contribute to disease pathogenesis. Although endothelial cells express angiotensin-converting enzyme 2 (ACE2), the relevance of endothelial-restricted viral tropism remains unclear. To directly assess the consequences of endothelial-restricted SARS-CoV-2 tropism , we generated a transgenic mouse model expressing human ACE2 under control of the endothelial-specific promoter (-hACE2). Despite confirmed pulmonary endothelial expression and protein presence of hACE2, SARS-CoV-2 infection of -hACE2 mice did not induce clinical illness, detectable viral replication, immune cell influx in the lung, or histopathological abnormalities in the lung or brain. These findings indicate that endothelial-restricted SARS-CoV-2 tropism alone is insufficient to drive productive infection and clinical disease , suggesting that endothelial involvement in COVID-19 likely arises in the context of broader cellular infection or systemic host responses rather than from primary endothelial infection. - Source: PubMed
Publication date: 2026/08/11
Lameire SahineDebeuf NincyDeckers JulieDe Wolf CarolineVanheerswynghels ManonToussaint WendyDe Vlieger LizeVan Hoecke LienBruggeman ArnoutDe Cae SieglindeSchepens BertVanhee StijnLambrecht Bart N - Internal N7-methylguanosine (mG) is a recently identified chemical modification of mammalian mRNA. Although the epitranscriptome plays a key role in regulating RNA metabolism and cellular function, the specific contribution of internal mG to cardiovascular disease remains unknown. Atherosclerosis preferentially develops at sites of disturbed blood flow, which promotes endothelial activation; however, whether internal mG regulates endothelial mechanotransduction and atherogenesis remains unclear. - Source: PubMed
Publication date: 2026/08/11
Shentu Tzu-PinWu TongZhou ZhengjieLi JinYeh Chih-FanZhu JiayuHuang Ru-TingMiao Bernadette AXi BrianLo JasonCarver LaurynLee Tzu-HanZhang LishengHarrison DevinHodonsky Chani JAuguste GaelleArasu Uma ThanigaiKaikkonen-Määttä MinnaHusain Aliya NTirrell Matthew VMiller Clint LDickinson Bryan CYang Kai-ChienFang Yun - We present a reproducible workflow for real-time visualization of nicotinamide adenine dinucleotide (NAD) biosensor-channel responses in brain microvascular endothelial cells in living mice using cranial-window two-photon microscopy and an endothelial-targeted fluorescent NAD sensor. The protocol includes (1) adeno-associated virus (AAV)-mediated expression of the NAD sensor selectively in cerebrovascular endothelium using AAV-X1.1 under the Cdh5 promoter (vascular endothelial cadherin), (2) surgical preparation of a stable 3 mm × 3 mm cortical cranial window, and (3) dual-wavelength two-photon imaging to simultaneously capture the 920 nm-excited green sensor-channel signal and the 1040 nm-excited intravascular tetramethylrhodamine (TMR)-dextran reference channel. The TMR-dextran channel provides a vascular lumen reference and supports vessel selection, motion assessment, and vascular-integrity evaluation. As an application example, we describe nicotinamide mononucleotide-associated changes in endothelial sensor-channel fluorescence following drinking-water, oral-gavage, or intravenous delivery. This protocol emphasizes critical steps, recommended viral-dosing and titer considerations, troubleshooting, and quantitative-analysis strategies, enabling laboratories to implement in vivo monitoring of cerebrovascular NAD biosensor-channel dynamics for studies of neurometabolism in health and disease. - Source: PubMed
Publication date: 2026/07/24
Zhan RuiLi YanyanMeng XiaCui HongtuZhao MingmingShan WenxinCao HuanhuanDu JianyongZhang JunxiaFang LuLi WenguangHe QihuaWang XinYang ZhaoSun JinpengZhang YouyiDong ErdanXiao Han - Endothelial dysfunction is critical for the pathogenesis of atherosclerosis, particularly in arterial regions exposed to disturbed flow (DF). ADCY4 (adenylate cyclase 4) catalyzes the production of cAMP, a ubiquitous second messenger that regulates cellular and physiological processes. This study investigated ADCY4 as a shear-stress-responsive gene in ECs for the regulation of vascular endothelial inflammation during atherogenesis. - Source: PubMed
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