Last update 01 Nov 2024

DNM1

Last update 01 Nov 2024

Basic Info

Synonyms

DNM, DNM1, dynamin 1

+ [1]

Introduction

Microtubule-associated force-producing protein involved in producing microtubule bundles and able to bind and hydrolyze GTP. Most probably involved in vesicular trafficking processes. Involved in receptor-mediated endocytosis.

Drugs associated with DNM1

Dynasore

Target

DNM1 x DNM2

Mechanism

DNM1 inhibitors [+1]

Active Org.

Harvard Medical School

Originator Org.

Harvard Medical School

Active Indication-

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with DNM1

100 Translational Medicine associated with DNM1

0 Patents (Medical) associated with DNM1

634

Literatures (Medical) associated with DNM1

01 Dec 2024·Cellular and Molecular Neurobiology

The Potential of Targeting Autophagy-Related Non-coding RNAs in the Treatment of Alzheimer’s and Parkinson’s Diseases

Review

Author: Golshadi, Zakieh ; Tamtaji, Zeinab ; Talebi Taheri, Abdolkarim ; Faghihi, Zahra ; Alinaghipour, Azam ; Nabavizadeh, Fatemeh ; Zare, Hamidreza ; Mirzaei, Hamed ; Dadgostar, Ehsan ; Tamtaji, Omid Reza ; Aschner, Michael

AbstractClearance of accumulated protein aggregates is one of the functions of autophagy. Recently, a clearer understanding of non-coding RNAs (ncRNAs) functions documented that ncRNAs have important roles in several biological processes associated with the development and progression of neurodegenerative disorders. Subtypes of ncRNA, including microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA), are commonly dysregulated in neurodegenerative disorders such as Alzheimer and Parkinson diseases. Dysregulation of these non-coding RNAs has been associated with inhibition or stimulation of autophagy. Decreased miR-124 led to decreased/increased autophagy in experimental model of Alzheimer and Parkinson diseases. Increased BACE1-AS showed enhanced autophagy in Alzheimer disease by targeting miR-214-3p, Beclin-1, LC3-I/LC3-II, p62, and ATG5. A significant increase in NEAT1led to stimulated autophagy in experimental model of PD by targeting PINK1, LC3-I, LC3-II, p62 and miR-374c-5p. In addition, increased BDNF-AS and SNHG1 decreased autophagy in MPTP-induced PD by targeting miR-125b-5p and miR-221/222, respectively. The upregulation of circNF1-419 and circSAMD4A resulted in an increased autophagy by regulating Dynamin-1 and miR-29c 3p, respectively. A detailed discussion of miRNAs, circRNAs, and lncRNAs in relation to their autophagy-related signaling pathways is presented in this study.Graphical AbstractAutophagy-related non-coding RNAs in neurodegenerative diseases.

01 Dec 2024·Journal of Trace Elements in Medicine and Biology

Molecular and immunohistochemical alterations in fluoride-induced neurological impediment in adult rats

Article

Author: Bhushan, Rashmi ; Chhabra, Vishal ; Shenoy, Smita ; Swamy, Ravindra Shantakumar ; Singh, Shubhankar Kumar ; Kumar, Nitesh ; Murti, Krishna ; Kumar, Sachindra

This study highlights the potential neurotoxic and impaired behavioral effects associated with high fluoride concentrations in drinking water.PURPOSEFluoride is known to cause neurotoxicity, evinced by lower I.Q. levels in children from high-fluoride regions as compared to those in low-fluoride regions. Thus, the present study was designed to investigate the molecular mechanism behind the neurological and behavioural changes induced by sodium fluoride in Wistar rats.MATERIAL AND METHODSA total of 24 female Wistar rats, aged six weeks and weighing approximately 150-220 g, were randomly divided into three groups: Group I (control) received reverse osmosis (R.O.) water, Group II received Sodium Fluoride (NaF) at 10 ppm, and Group III received NaF at 50 ppm in their drinking water for 60 days. The animals underwent behavioural tests including the Forced Swim Test (F.S.T.), Open Field Test (OFT), and Novel Object Recognition Test (N.O.R.T.), to assess any alterations in behaviour. After 60 days, the animals were euthanized, and their blood and brain samples were analysed to evaluate biochemical changes by Western Blot/I.H.C. analysis of B.A.X., Bcl2, LC3B, TLR4, PARP1, p53, Caspase, α-Synuclein, PARKIN, NeuN, KI67, DNM-1, and M.F.N. for assessing molecular pathways for toxicity.RESULTSImpaired locomotion, memory impairment, and behaviour resembling depression in the animals were evinced by reduced mobility index in the F.S.T., discrimination index in the N.O.R.T., and reduced locomotor activity in the open field test results. Additionally, alterations in antioxidant levels and oxidative stress parameters were observed in the brain. The expression levels of various apoptotic and inflammatory biomarkers (B.A.X., Bcl2, TLR4, PARP1, p53, and Caspase) showed apoptosis in neurons. The confocal studies showed increased expression of inflammatory (α-Synuclein, PARKIN), apoptotic (LC3B, B.A.X., p53, KI67), and mitochondrial dysfunction (NeuN, DNM-1, M.F.N.) markers in fluoride-treated animals. Toxicity was more prominent in 50 ppm of fluoride-treated animals.CONCLUSIONFluoride showed potent neuronal toxicity as evidenced by alterations of various molecular markers.

02 Oct 2024·Autophagy

Atg44/Mdi1/mitofissin facilitates Dnm1-mediated mitochondrial fission

Article

Author: Hayatsu, Manabu ; Inoue, Keiichi ; Okuyama, Kentaro ; Fukuda, Tomoyuki ; Furukawa, Kentaro ; Shibata, Shinsuke ; Kanki, Tomotake ; Yamashita, Shun-Ichi

Mitochondria undergo fission and fusion, and their coordinated balance is crucial for maintaining mitochondrial homeostasis. In yeast, the dynamin-related protein Dnm1 is a mitochondrial fission factor acting from outside the mitochondria. We recently reported the mitochondrial intermembrane space protein Atg44/mitofissin/Mdi1/Mco8 as a novel fission factor, but the relationship between Atg44 and Dnm1 remains elusive. Here, we show that Atg44 is required to complete Dnm1-mediated mitochondrial fission under homeostatic conditions. Atg44-deficient cells often exhibit enlarged mitochondria with accumulated Dnm1 and rosary-like mitochondria with Dnm1 foci at constriction sites. These mitochondrial constriction sites retain the continuity of both the outer and inner membranes within an extremely confined space, indicating that Dnm1 is unable to complete mitochondrial fission without Atg44. Moreover, accumulated Atg44 proteins are observed at mitochondrial constriction sites. These findings suggest that Atg44 and Dnm1 cooperatively execute mitochondrial fission from inside and outside the mitochondria, respectively.Abbreviation: ATG: autophagy related; CLEM: correlative light and electron microscopy; EM: electron microscopy; ER: endoplasmic reticulum; ERMES: endoplasmic reticulum-mitochondria encounter structure; GA: glutaraldehyde; GFP: green fluorescent protein; GTP: guanosine triphosphate: IMM: inner mitochondrial membrane; IMS: intermembrane space; OMM: outer mitochondrial membrane; PB: phosphate buffer; PBS: phosphate-buffered saline; PFA: paraformaldehyde; RFP: red fluorescent protein; WT: wild type.

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