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Ovarian Kaleidoscope Database (OKdb)

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Dipeptidase 3 OKDB#: 3911
 Symbols: DPEP3 Species: human
 Synonyms: MBD3,MEMBRANE-BOUND DIPEPTIDASE 3, MBD3  Locus: 16q22.1 in Homo sapiens


For retrieval of Nucleotide and Amino Acid sequences please go to: OMIM Entrez Gene
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link to BioGPS
General Comment NCBI Summary: This gene encodes a membrane-bound glycoprotein from the family of dipeptidases involved in hydrolytic metabolism of various dipeptides, including penem and carbapenem beta-lactam antibiotics. This gene is located on chromosome 16 in a cluster with another member of this family. Alternatively spliced transcript variants that encode different isoforms have been found for this gene. [provided by RefSeq]
General function Enzyme
Comment
Cellular localization
Comment
Ovarian function
Comment Whole transcriptome analysis of the effects of type I diabetes on mouse oocytes. Ma JY et al. In mouse ovarian follicles, granulosa cells but not oocytes take up glucose to provide the oocyte with nourishments for energy metabolism. Diabetes-induced hyperglycemia or glucose absorption inefficiency consistently causes granulosa cell apoptosis and further exerts a series of negative impacts on oocytes including reduced meiosis resumption rate, low oocyte quality and preimplantation embryo degeneration. Here we compared the transcriptome of mouse oocytes from genetically derived NOD diabetic mice or chemically induced STZ diabetic mice with that of corresponding normal mice. Differentially expressed genes were extracted from the two diabetic models. Gene set enrichment analysis showed that genes associated with metabolic and developmental processes were differentially expressed in oocytes from both models of diabetes. In addition, NOD diabetes also affected the expression of genes associated with ovulation, cell cycle progression, and preimplantation embryo development. Notably, Dnmt1 expression was significantly down-regulated, but Mbd3 expression was up-regulated in diabetic mouse oocytes. Our data not only revealed the mechanisms by which diabetes affects oocyte quality and preimplantation embryo development, but also linked epigenetic hereditary factors with metabolic disorders in germ cells.
Expression regulated by
Comment
Ovarian localization Oocyte
Comment Genomewide discovery and classification of candidate ovarian fertility genes in the mouse. Gallardo TD et al. Female infertility syndromes are among the most prevalent chronic health disorders in women, but their genetic basis remains unknown because of uncertainty regarding the number and identity of ovarian factors controlling the assembly, preservation, and maturation of ovarian follicles. To systematically discover ovarian fertility genes en masse, we employed a mouse model (Foxo3) in which follicles are assembled normally but then undergo synchronous activation. We developed a microarray-based approach for the systematic discovery of tissue-specific genes and, by applying it to Foxo3 ovaries and other samples, defined a surprisingly large set of ovarian factors (n = 348, approximately 1% of the mouse genome). This set included the vast majority of known ovarian factors, 44% of which when mutated produce female sterility phenotypes, but most were novel. Comparative profiling of other tissues, including microdissected oocytes and somatic cells, revealed distinct gene classes and provided new insights into oogenesis and ovarian function, demonstrating the utility of our approach for tissue-specific gene discovery. This study will thus facilitate comprehensive analyses of follicle development, ovarian function, and female infertility. This is an oocyte-specific gene.
Follicle stages
Comment
Phenotypes
Mutations 0 mutations
Genomic Region show genomic region
Phenotypes and GWAS show phenotypes and GWAS
Links
OMIM (Online Mendelian Inheritance in Man: an excellent source of general gene description and genetic information.)
OMIM \ Animal Model
KEGG Pathways
Recent Publications
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created: Jan. 27, 2009, 4:51 p.m. by: hsueh   email:
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last update: Aug. 24, 2012, 10:01 a.m. by: hsueh    email:



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