NRKs TV-kanaler direkte på nett.

NRK2 (pronounced as "NRK to") is one of the television channels of the Norwegian Broadcasting Corporation (NRK). It was launched on 1 September 1996. [1] The channel started its regular broadcasts on 1 September 1996, but on the evening before, a live simulcast, led by Trond-Viggo Torgersen, was broadcast on NRK1 and NRK2.

2024年12月25日 · NMRK2 (Nicotinamide Riboside Kinase 2) is a Protein Coding gene. Diseases associated with NMRK2 include Muscular Dystrophy, Congenital, Due To Integrin Alpha-7 Deficiency and Dilated Cardiomyopathy. Among its related pathways are Metabolism of water-soluble vitamins and cofactors and NAD metabolism.

2024年12月1日 · Nicotinamide riboside kinase-2 (NRK-2 or NMRK2) is a muscle-specific β1-integrin binding protein abundantly expressed in the skeletal muscle while only a trace amount is detected in the healthy cardiac muscle. The level in cardiac tissue is profoundly upregulated under pathogenic conditions such as ischemia and hypertension.

2016年10月11日 · NRKs, encoded by the Nmrk genes, are highly conserved enzymes in all eukaryotes 18. In mammals there are two NRK enzymes, NRK1 and NRK2, but little is known about their physiological roles. In...

挪威廣播公司第二台（挪威語：nrk2）是挪威廣播公司一條於1996年開播的電視頻道，主要播放新聞、戲劇和文化節目。 這條頻道曾經擁有一個名為「Svisj」的節目板塊，其內容包含音樂錄影帶以及簡訊聊天交流節目，不過這個板塊已經在2007年9月移至新成立的 ...

启用核糖基烟酰胺激酶活性和核糖基烟酸激酶活性。 预计参与 NAD 代谢过程。 预计在成肌细胞分化的负调节上游或负调节内起作用。 位于核质和质膜中。 [由基因组资源联盟提供，2022 年 4 月] Enables ribosylnicotinamide kinase activity and ribosylnicotinate kinase activity. Predicted to be involved in NAD metabolic process. Predicted to act upstream of or within negative regulation of myoblast differentiation.

Catalyzes the phosphorylation of nicotinamide riboside (NR) and nicotinic acid riboside (NaR) to form nicotinamide mononucleotide (NMN) and nicotinic acid mononucleotide (NaMN). Reduces laminin matrix deposition and cell adhesion to laminin, but not to fibronectin.

2020年3月1日 · NRK-2 protects heart from dilatative cardiac remodeling post-ischemia. Loss of NRK-2 promotes post-MI scar expansion and thinning, fibrosis, LV dilatation, and heart failure. Gain of NRK-2 function limits hypoxia re-oxygenation -induced cardiomyopathy. NRK-2 specifically inhibits p38α activation to protect heart from ischemic insult.

Mechanistically, we identified NRK-2 as a regulator of c-jun N-terminal kinase (JNK) MAP kinase and mitochondrial function where NRK-2 overexpression in human cardiomyocytes markedly suppressed the Ang II-induced JNK activation and mitochondrial depolarization.