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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Mitofusin 2

HSG, Mfn2, mitofusin 2
This gene encodes a mitochondrial membrane protein that participates in mitochondrial fusion and contributes to the maintenance and operation of the mitochondrial network. This protein is involved in the regulation of vascular smooth muscle cell proliferation, and it may play a role in the pathophysiology of obesity. Mutations in this gene cause Charcot-Marie-Tooth disease type 2A2, and hereditary motor and sensory neuropathy VI, which are both disorders of the peripheral nervous system. Defects in this gene have also been associated with early-onset stroke. Two transcript variants encoding the same protein have been identified. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, HAD, ACID, CMT2, V1a
Papers using HSG antibodies
The cleaved-Caspase-3 antibody is a marker of Caspase-9-like DRONC activity in Drosophila
Supplier
Kornbluth S et al., In Cell Death and Differentiation, 2009
... GFP-Drp1K38A and GFP-MFN2 were generated by cloning hDrp1K38A and hMFN2 into pEGFP-C1 (Clontech, Mountain View, CA, USA), ...
Papers on HSG
Mitofusin 2 maintains haematopoietic stem cells with extensive lymphoid potential.
New
Impact
Snoeck et al., New York City, United States. In Nature, Feb 2016
Here we show in mice that the short isoform of a critical regulator of HSCs, Prdm16 (refs 4, 5), induces mitofusin 2 (Mfn2), a protein involved in mitochondrial fusion and in tethering of mitochondria to the endoplasmic reticulum.
Transcriptional profiling revealed the anti-proliferative effect of MFN2 deficiency and identified risk factors in lung adenocarcinoma.
New
Han et al., Shanghai, China. In Tumour Biol, Feb 2016
UNASSIGNED: Mitofusin-2 (MFN2) was initially identified as a hyperplasia suppressor in hyper-proliferative vascular smooth muscle cells (VSMCs) of hypertensive rat arteries, which has also been implicated in various cancers.
[Pathology of Charcot-Marie-Tooth Disease].
Review
New
Oka, Kyoto, Japan. In Brain Nerve, Jan 2016
CMT2A (MFN2 mutation) shows abnormal mitochondria with a spherical morphology instead of tubular in the longitudinal direction.
Defective DNA methylation in salivary gland epithelial acini from patients with Sjögren's syndrome is associated with SSB gene expression, anti-SSB/LA detection, and lymphocyte infiltration.
New
Renaudineau et al., Brest, France. In J Autoimmun, Jan 2016
The effect of the DNA demethylating drug 5 azacytidine (5-Aza) was tested in the human salivary gland (HSG) cell line.
Dengue Virus Impairs Mitochondrial Fusion by Cleaving Mitofusins.
New
Lin et al., Tainan City, Taiwan. In Plos Pathog, Dec 2015
Two mitofusins (MFN1 and MFN2), which mediate mitochondrial fusion and participate in the proper function of mitochondria, were cleaved by DENV protease NS2B3.
Pro-apoptotic and anti-proliferative effects of mitofusin-2 via PI3K/Akt signaling in breast cancer cells.
New
Liu et al., Shijiazhuang, China. In Oncol Lett, Dec 2015
UNASSIGNED: The mitochondrial GTPase mitofusin-2 (Mfn2) gene is a novel gene characterized as a cell proliferation inhibitor.
FOXO1 and GSK-3β Are Main Targets of Insulin-Mediated Myogenesis in C2C12 Muscle Cells.
New
Orzechowski et al., Warsaw, Poland. In Plos One, Dec 2015
Insulin-dependent myogenesis was accompanied by the rise of mtTFA, MtSSB, Mfn2, and mitochondrially encoded Cox-1 gene expressions and elevated levels of proteins which control functions of mitochondria (kinase-PKB/AKT, mitofusin 2 protein-Mfn-2).
MFN2-related neuropathies: Clinical features, molecular pathogenesis and therapeutic perspectives.
Review
New
Corti et al., Milano, Italy. In J Neurol Sci, Oct 2015
Mitofusin 2 (MFN2) is a GTPase dynamin-like protein of the outer mitochondrial membrane, encoded in the nuclear genome by the MFN2 gene located on the short (p) arm of chromosome 1.
Mutations in SLC25A46, encoding a UGO1-like protein, cause an optic atrophy spectrum disorder.
New
Impact
Dallman et al., Miami, United States. In Nat Genet, Aug 2015
Dominant optic atrophy (DOA) and axonal peripheral neuropathy (Charcot-Marie-Tooth type 2, or CMT2) are hereditary neurodegenerative disorders most commonly caused by mutations in the canonical mitochondrial fusion genes OPA1 and MFN2, respectively.
Mitochondrial dynamics and inherited peripheral nerve diseases.
Review
New
Piscosquito et al., Milano, Italy. In Neurosci Lett, Jul 2015
Abnormalities of mitochondrial dynamics produced by mutations in proteins involved in mitochondrial fusion (mitofusin-2, MFN2), fission (ganglioside-induced differentiation-associated protein-1, GDAP1), and mitochondrial axonal transport usually present with a Charcot-Marie-Tooth disease (CMT) phenotype.
Mitochondrial dynamics in pulmonary arterial hypertension.
Review
New
Archer et al., Salt Lake City, United States. In J Mol Med (berl), Mar 2015
The molecular basis of this structural change includes upregulation and activation of fission mediators, notably dynamin-related protein 1 (DRP-1), and downregulation of fusion mediators, especially mitofusin-2 (MFN2).
Implications of mitochondrial dynamics on neurodegeneration and on hypothalamic dysfunction.
Review
Claret et al., Barcelona, Spain. In Front Aging Neurosci, 2014
Mutations in two mitochondrial fusion genes (MFN2 and OPA1) cause neurodegenerative diseases, namely Charcot-Marie Tooth type 2A and autosomal dominant optic atrophy (ADOA).
Mitochondrial dynamics controlled by mitofusins regulate Agrp neuronal activity and diet-induced obesity.
Impact
Horvath et al., New Haven, United States. In Cell, 2013
Interfering with mitochondrial fusion mechanisms in Agrp neurons by cell-selectively knocking down mitofusin 1 (Mfn1) or mitofusin 2 (Mfn2) resulted in altered mitochondria size and density in these cells.
Mitofusin 2 in POMC neurons connects ER stress with leptin resistance and energy imbalance.
Impact
Claret et al., Barcelona, Spain. In Cell, 2013
Mitofusin 2 (MFN2) plays critical roles in both mitochondrial fusion and the establishment of mitochondria-endoplasmic reticulum (ER) interactions.
PINK1-phosphorylated mitofusin 2 is a Parkin receptor for culling damaged mitochondria.
Impact
Dorn et al., Saint Louis, United States. In Science, 2013
Parkin bound to Mfn2 in a PINK1-dependent manner; PINK1 phosphorylated Mfn2 and promoted its Parkin-mediated ubiqitination.
Central role of mitofusin 2 in autophagosome-lysosome fusion in cardiomyocytes.
GeneRIF
Zheng et al., Beijing, China. In J Biol Chem, 2012
Data indicate that eficiency of mitofusin 2 (MFN2) caused multiple molecular and functional defects that undermined cardiac reserve and gradually led to cardiac vulnerability and dysfunction.
Up-regulation of mitofusin-2 protects CD4+ T cells from HMGB1-mediated immune dysfunction partly through Ca(2+)-NFAT signaling pathway.
GeneRIF
Sheng et al., Wenzhou, China. In Cytokine, 2012
HMGB1 have a direct role on adaptive immunity, and the decrease of Mfn2 expression may be a major cause of HMGB1-mediated immune dysfunction and Ca(2+)-NFAT signaling defect of CD4(+) T lymphocytes.
Loss of mitofusin 2 promotes endoplasmic reticulum stress.
GeneRIF
Walsh et al., Boston, United States. In J Biol Chem, 2012
Mfn2 but not Mfn1 is an ER stress-inducible protein that is required for the proper temporal sequence of the ER stress response.
Hepatitis B virus X protein inhibits p53-mediated upregulation of mitofusin-2 in hepatocellular carcinoma cells.
GeneRIF
Zheng et al., Hangzhou, China. In Biochem Biophys Res Commun, 2012
These results indicate that HBx impacts p53-mediated transcription of Mfn2, providing insight into the negative effect of HBx against p53-dependent chemotherapeutic agents, such as doxorubicin, used in the treatment of hepatocellular carcinoma.
A novel mutation of the MFN2 gene in a Chinese family with Charcot-Marie-Tooth disease.
GeneRIF
Li et al., Shenyang, China. In Genet Mol Res, 2011
Data revealed a missense mutation (NM_014874.3:c.1066 A>G) in the MFN2 gene, resulting in an animo acid substitution of threonine to alanine in condon 356 (Thr356Ala). This is a novel phenotype and mutation for Charcot-Marie-Tooth family.
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