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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Electron-transferring-flavoprotein dehydrogenase

MADD, ETFDH, DENN, ETF-QO, IG20, ETFB
Electron-transferring-flavoprotein dehydrogenase in the inner mitochondrial membrane accepts electrons from electron-transfer flavoprotein which is located in the mitochondrial matrix and reduces ubiquinone in the mitochondrial membrane. The protein is synthesized as a 67-kDa precursor which is targeted to mitochondria and processed in a single step to a 64-kDa mature form located in the mitochondrial membrane. Deficiency in electron-transferring-flavoprotein dehydrogenase have been demonstrated in some patients with type II glutaricacidemia. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ETF, CAN, ACID, oxidoreductase, HAD
Papers on MADD
Regulation of T Cell Receptor Signaling by DENND1B in TH2 Cells and Allergic Disease.
New
Impact
Chan et al., San Francisco, United States. In Cell, Feb 2016
The DENN domain is an evolutionary conserved protein module found in all eukaryotes and serves as an exchange factor for Rab-GTPases to regulate diverse cellular functions.
Downregulation of miR-522 suppresses proliferation and metastasis of non-small cell lung cancer cells by directly targeting DENN/MADD domain containing 2D.
New
Zhang et al., Harbin, China. In Sci Rep, Dec 2015
In addition, a luciferase assay identified DENN/MADD domain containing 2D (DENND2D) as a direct target of miR-522.
Lst4, the yeast Fnip1/2 orthologue, is a DENN-family protein.
New
Blundell et al., Villejuif, France. In Open Biol, Dec 2015
Lst4 has been previously proposed to be the Fnip1/2 orthologue in yeast and therefore a member of the DENN family.
Epigenetic silencing of tumor suppressor miR-3151 contributes to Chinese chronic lymphocytic leukemia by constitutive activation of MADD/ERK and PIK3R2/AKT signaling pathways.
New
Chim et al., Hong Kong, Hong Kong. In Oncotarget, Nov 2015
Luciferase assay confirmed MAP-kinase activating death domain (MADD) and phosphoinositide-3-kinase, regulatory subunit 2 (PIK3R2) as direct targets of miR-3151.
Inhibition of glial proliferation, promotion of axonal growth and myelin production by synthetic glycolipid: A new approach for spinal cord injury treatment.
New
Doncel-Pérez et al., Toledo, Spain. In Restor Neurol Neurosci, Nov 2015
Recently, we have described a synthetic glycolipid (IG20) that inhibited proliferation of human glioma cells.
Bent spine syndrome as an initial manifestation of late-onset multiple acyl-CoA dehydrogenase deficiency: a case report and literature review.
Review
Hong et al., Nanchang, China. In Bmc Neurol, 2014
BACKGROUND: Late-onset multiple acyl-CoA dehydrogenase deficiency (MADD) is an autosomal recessive inherited disease of metabolic dysfunction clinically characterized by fluctuating proximal muscle weakness, excise intolerance, and dramatic riboflavin responsiveness.
Cardanol isolated from Thai Apis mellifera propolis induces cell cycle arrest and apoptosis of BT-474 breast cancer cells via p21 upregulation.
Chanchao et al., Bangkok, Thailand. In Daru, 2014
Moreover, cardanol changed the transcript expression levels of genes involved in the control of apoptosis (increased DR5 and Bcl-2 expression and decreased Mcl-1, MADD and c-FLIPP) and cell division (increased p21 and E2FI and decreased cyclin D1, cyclin E, CDK4 and CDK2 expression), as well as increasing the level of p21 p-ERK, p-JNK and p-p38 and decreasing cyclin D. This accounts for the failure to progress from the G1 to the S subphase.
Riboflavin-responsive multiple Acyl-CoA dehydrogenation deficiency in 13 cases, and a literature review in mainland Chinese patients.
Review
Hong et al., Nanchang, China. In J Hum Genet, 2014
Multiple Acyl-CoA dehydrogenation deficiency (MADD) is an autosomal recessive disorder of fatty acid oxidation and amino-acid metabolism.
Exome array analysis identifies new loci and low-frequency variants influencing insulin processing and secretion.
Impact
Mohlke et al., Ann Arbor, United States. In Nat Genet, 2013
We identified low-frequency coding variants associated with fasting proinsulin concentrations at the SGSM2 and MADD GWAS loci and three new genes with low-frequency variants associated with fasting proinsulin or insulinogenic index: TBC1D30, KANK1 and PAM.
Splice variants in apoptotic pathway.
Review
Unno et al., Sendai, Japan. In Exp Oncol, 2012
In this article we summarized splice variants of some of the apoptotic genes including BCL2L1, BIRC5, CFLAR, and MADD, as well as the regulatory mechanisms of alternative splicing of these genes.
Mechanism of superoxide and hydrogen peroxide generation by human electron-transfer flavoprotein and pathological variants.
GeneRIF
Gomes et al., Lisbon, Portugal. In Free Radic Biol Med, 2012
Point mutations in electron-transfer-flavoprotein beta is associated with destabilized conformations and defective protein:protein interactions leading to mitochondrial dysfunction.
Update on clinical aspects and treatment of selected vitamin-responsive disorders II (riboflavin and CoQ 10).
Review
Horvath, Newcastle upon Tyne, United Kingdom. In J Inherit Metab Dis, 2012
Mutations in the electron tranferring fravoprotein genes (ETFA/ETFB) and its dehydrogenase (ETFDH) are causative for multiple acyl-CoA dehydrogenase deficiency.
[Expression of MADD in lung adenocarcinoma tissues and its effects on proliferation and apoptosis of lung adenocarcinoma A549 cells].
GeneRIF
Dong et al., Jinan, China. In Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi, 2012
Data show that ehe expression of MAPK-activating death domain protein (MADD) increases obviously in lung adenocarcinoma, and MADD can promote survival of lung adenocarcinoma cells by inhibiting apoptosis.
Cardiac myosin binding protein C and MAP-kinase activating death domain-containing gene polymorphisms and diastolic heart failure.
GeneRIF
Tsai et al., Taipei, Taiwan. In Plos One, 2011
SNP rs2290149, located in a genetic cluster of MYBPC3 and MADD gene, was found to be associated with diastolic heart failure.
Identification of ETFB as a candidate protein that participates in the mechanoregulation of fibroblast cell number in collagen gel culture.
GeneRIF
Shimosaka et al., Yokohama, Japan. In J Dermatol Sci, 2011
ETFB participates in the mechanoregulation of fibroblast cell number in collagen gel culture.
DENN domain proteins: regulators of Rab GTPases.
Review
McPherson et al., Montréal, Canada. In J Biol Chem, 2011
The DENN domain is a common, evolutionarily ancient, and conserved protein module, yet it has gone largely unstudied; until recently, little was known regarding its functional roles.
Glucose-raising genetic variants in MADD and ADCY5 impair conversion of proinsulin to insulin.
GeneRIF
Fritsche et al., Tübingen, Germany. In Plos One, 2010
The SNP in ADCY5 is implicated in defective proinsulin-to-insulin conversion and previous findings on the role of a genetic variant in MADD on proinsulin-to-insulin conversion, were confirmed.
New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.
Impact
Barroso et al., Boston, United States. In Nat Genet, 2010
These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1).
A genome-wide perspective of genetic variation in human metabolism.
Impact
Suhre et al., München, Germany. In Nat Genet, 2010
For eight out of nine replicated loci (FADS1, ELOVL2, ACADS, ACADM, ACADL, SPTLC3, ETFDH and SLC16A9), the genetic variant is located in or near genes encoding enzymes or solute carriers whose functions match the associating metabolic traits.
KIF1Bbeta- and KIF1A-mediated axonal transport of presynaptic regulator Rab3 occurs in a GTP-dependent manner through DENN/MADD.
Impact
GeneRIF
Hirokawa et al., Tokyo, Japan. In Nat Cell Biol, 2008
KIF1Bbeta- and KIF1A-mediated axonal transport of presynaptic regulator Rab3 occurs in a GTP-dependent manner through MADD.
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