10-[2-DIETHYLAMINOPROPYL]PHENOTHIAZINE

10-[2-DIETHYLAMINOPROPYL]PHENOTHIAZINE Structure
10-[2-DIETHYLAMINOPROPYL]PHENOTHIAZINE structure
Common Name 10-[2-DIETHYLAMINOPROPYL]PHENOTHIAZINE
CAS Number 1094-08-2 Molecular Weight 348.93300
Density N/A Boiling Point 430.1ºC at 760 mmHg
Molecular Formula C19H25ClN2S Melting Point 225 - 228 °C
MSDS Chinese USA Flash Point 213.9ºC
Symbol GHS07
GHS07
Signal Word Warning

Binding to serine 65-phosphorylated ubiquitin primes Parkin for optimal PINK1-dependent phosphorylation and activation.

EMBO Rep. 16 , 939-54, (2015)

Mutations in the mitochondrial protein kinase PINK1 are associated with autosomal recessive Parkinson disease (PD). We and other groups have reported that PINK1 activates Parkin E3 ligase activity both directly via phosphorylation of Parkin serine 65 (Ser(65)...

Characterization of Species Differences in Tissue Diltiazem Deacetylation Identifies Ces2a as a Rat-Specific Diltiazem Deacetylase.

Drug Metab. Dispos. 43 , 1218-25, (2015)

Diltiazem, a calcium channel blocker, is mainly metabolized via demethylation or deacetylation in humans. Diltiazem demethylation is catalyzed by cytochrome P450 2D6 and 3A4. Although it was previously reported that the area under the curve ratio of deacetyld...

Linking a compound-heterozygous Parkin mutant (Q311R and A371T) to Parkinson's disease by using proteomic and molecular approaches.

Neurochem. Int. 85-86 , 1-13, (2015)

Parkin is an E3-protein ubiquitin ligase, which plays an important role as a scavenger in cell metabolism. Since the discovery of the link between Parkin and Parkinson's disease, Parkin was placed in the center of Parkinson's disease research. Previously, we ...

Phosphorylated ubiquitin chain is the genuine Parkin receptor.

J. Cell Biol. 209(1) , 111-28, (2015)

PINK1 selectively recruits Parkin to depolarized mitochondria for quarantine and removal of damaged mitochondria via ubiquitylation. Dysfunction of this process predisposes development of familial recessive Parkinson's disease. Although various models for the...

Expression pattern of parkin isoforms in lung adenocarcinomas.

Tumour Biol. 36 , 5133-41, (2015)

The parkin gene has been shown to be genetically altered in a wide variety of human tumors including lung cancer. Although many parkin splice variants have been identified, to date, most of the studies have only been focused on originally cloned isoforms. In ...

Parkin-mediated K63-polyubiquitination targets ubiquitin C-terminal hydrolase L1 for degradation by the autophagy-lysosome system.

Cell. Mol. Life Sci. 72(9) , 1811-24, (2015)

Ubiquitin C-terminal hydrolase L1 (UCH-L1) is a key neuronal deubiquitinating enzyme which is mutated in Parkinson disease (PD) and in childhood-onset neurodegenerative disorder with optic atrophy. Furthermore, reduced UCH-L1 protein levels are associated wit...

Parkin-induced ubiquitination of Mff promotes its association with p62/SQSTM1 during mitochondrial depolarization.

Acta Biochim. Biophys. Sin. (Shanghai) 47 , 522-9, (2015)

The ubiquitin ligase Parkin and autophagic adapter protein p62 are known to function in a common pathway controlling mitochondrial autophagy (mitophagy). However, the evidence supporting that p62 is directly recruited by ubiquitinated proteins remains undeter...

Phosphorylation of mitochondrial polyubiquitin by PINK1 promotes Parkin mitochondrial tethering.

PLoS Genet. 10(12) , e1004861, (2014)

The kinase PINK1 and the E3 ubiquitin (Ub) ligase Parkin participate in mitochondrial quality control. The phosphorylation of Ser65 in Parkin's ubiquitin-like (UBl) domain by PINK1 stimulates Parkin activation and translocation to damaged mitochondria, which ...

Mesenchymal stem cells use extracellular vesicles to outsource mitophagy and shuttle microRNAs.

Nat. Commun. 6 , 8472, (2015)

Mesenchymal stem cells (MSCs) and macrophages are fundamental components of the stem cell niche and function coordinately to regulate haematopoietic stem cell self-renewal and mobilization. Recent studies indicate that mitophagy and healthy mitochondrial func...

Hepatitis C Virus Core Protein Suppresses Mitophagy by Interacting with Parkin in the Context of Mitochondrial Depolarization

Am. J. Pathol. 184(11) , 3026-39, (2014)

Hepatitis C virus (HCV) causes mitochondrial injury and oxidative stress, and impaired mitochondria are selectively eliminated through autophagy-dependent degradation (mitophagy). We investigated whether HCV affects mitophagy in terms of mitochondrial quality...