Редактирование: ACAD10 (раздел)

==Publications==

{{medline-entry
|title=Genome-wide association study and annotating candidate gene networks affecting age at first calving in Nellore cattle.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28994157
|abstract=We performed a genome-wide mapping for the age at first calving (AFC) with the goal of annotating candidate genes that regulate fertility in Nellore cattle. Phenotypic data from 762 cows and 777k SNP genotypes from 2,992 bulls and cows were used. Single nucleotide polymorphism (SNP) effects based on the single-step GBLUP methodology were blocked into adjacent windows of 1 Megabase (Mb) to explain the genetic variance. SNP windows explaining more than 0.40% of the AFC genetic variance were identified on chromosomes 2, 8, 9, 14, 16 and 17. From these windows, we identified 123 coding protein genes that were used to build gene networks. From the association study and derived gene networks, putative candidate genes (e.g., [[PAPPA]], [[PREP]], [[FER1L6]], [[TPR]], [[NMNAT1]], [[ACAD10]], [[PCMTD1]], [[CRH]], OPKR1, [[NPBWR1]] and NCOA2) and transcription factors (TF) (STAT1, [[STAT3]], [[RELA]], [[E2F1]] and EGR1) were strongly associated with female fertility (e.g., negative regulation of luteinizing hormone secretion, folliculogenesis and establishment of uterine receptivity). Evidence suggests that AFC inheritance is complex and controlled by multiple loci across the genome. As several windows explaining higher proportion of the genetic variance were identified on chromosome 14, further studies investigating the interaction across haplotypes to better understand the molecular architecture behind AFC in Nellore cattle should be undertaken.
|mesh-terms=* Aging
* Animals
* Breeding
* Cattle
* Female
* Fertility
* Gene Regulatory Networks
* Genome-Wide Association Study
* Genotype
* Phenotype
* Polymorphism, Single Nucleotide
* Quantitative Trait Loci
|keywords=* beef cattle
* gene function
* single-step
|full-text-url=https://sci-hub.do/10.1111/jbg.12299
}}
{{medline-entry
|title=Metformin: a metabolic modulator.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28122334
|abstract=Recent findings have shed new light on the mechanisms of action through which biguanides exert their anti-aging and cytostatic effects in Caenorhabditis elegans and human cell lines. The drop in energy charge resulting from the metformin mediated inhibition of mitochondrial activity affects the function of the nuclear pore complex, blocks mTOR signaling and enhances the expression of [[ACAD10]]. Whether the inhibition of this pathway is truly responsible for the anti-diabetic and cancer effects of the drug in mammals remains to be established.
|mesh-terms=* Acyl-CoA Dehydrogenase
* Animals
* Antineoplastic Agents
* Caenorhabditis elegans
* Caenorhabditis elegans Proteins
* Diabetes Mellitus, Type 2
* Energy Metabolism
* Humans
* Hypoglycemic Agents
* Metformin
* Mitochondria
* Neoplasms
* Signal Transduction
* TOR Serine-Threonine Kinases
|keywords=* aging
* autophagy
* biguanides
* caloric restriction
* cancer
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354711
}}
{{medline-entry
|title=An Ancient, Unified Mechanism for Metformin Growth Inhibition in C. elegans and Cancer.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27984722
|abstract=Metformin has utility in cancer prevention and treatment, though the mechanisms for these effects remain elusive. Through genetic screening in C. elegans, we uncover two metformin response elements: the nuclear pore complex (NPC) and acyl-CoA dehydrogenase family member-10 ([[ACAD10]]). We demonstrate that biguanides inhibit growth by inhibiting mitochondrial respiratory capacity, which restrains transit of the RagA-RagC GTPase heterodimer through the NPC. Nuclear exclusion renders RagC incapable of gaining the GDP-bound state necessary to stimulate mTORC1. Biguanide-induced inactivation of mTORC1 subsequently inhibits growth through transcriptional induction of [[ACAD10]]. This ancient metformin response pathway is conserved from worms to humans. Both restricted nuclear pore transit and upregulation of [[ACAD10]] are required for biguanides to reduce viability in melanoma and pancreatic cancer cells, and to extend C. elegans lifespan. This pathway provides a unified mechanism by which metformin kills cancer cells and extends lifespan, and illuminates potential cancer targets. PAPERCLIP.
|mesh-terms=* Acyl-CoA Dehydrogenase
* Aging
* Animals
* Body Size
* Caenorhabditis elegans
* Caenorhabditis elegans Proteins
* Cell Line, Tumor
* DNA-Binding Proteins
* Humans
* Longevity
* Mechanistic Target of Rapamycin Complex 1
* Metformin
* Mitochondria
* Monomeric GTP-Binding Proteins
* Multiprotein Complexes
* Neoplasms
* Nuclear Pore
* Oxidative Phosphorylation
* Signal Transduction
* TOR Serine-Threonine Kinases
* Transcription Factors
|keywords=* ACAD10
* C. elegans
* Metformin
* NPC
* RagC GTPase
* acyl-CoA dehydrogenase family member 10
* cancer
* diabetes
* growth
* lifespan
* mTORC1
* mechanistic target of rapamycin complex 1
* mitochondrial respiratory capacity
* nuclear pore complex
* nuclear transport
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5390486
}}
{{medline-entry
|title=Metformin: Restraining Nucleocytoplasmic Shuttling to Fight Cancer and Aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27984715
|abstract=In this issue of Cell, Wu et al. employed C. elegans and human cell experiments to identify a pathway through which metformin increases lifespan and inhibits growth. A key transcriptional target, [[ACAD10]], is activated when metformin induces nuclear exclusion of the GTPase RagC, thereby inhibiting mTORC1 through an unexpected mechanism.
|mesh-terms=* Active Transport, Cell Nucleus
* Aging
* Animals
* Caenorhabditis elegans
* Humans
* Metformin
* Neoplasms

|full-text-url=https://sci-hub.do/10.1016/j.cell.2016.11.058
}}