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Pleiotrophin OKDB#: 1029
 Symbols: PTN Species: human
 Synonyms: NEURITE OUTGROWTH-PROMOTING FACTOR, HEPARIN-BINDING| NEURITE GROWTH-PROMOTING FACTOR 1, NEGF1| HEPARIN-BINDING GROWTH FACTOR 8, HBGF8|  Locus: 7q33 in Homo sapiens


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General Comment Pleiotropin/Heparin-binding neurite outgrowth-promoting factor is a member of a highly conserved human gene family of proteins. It exhibits neurite outgrowth-promoting activity and may play a role in nervous tissue development and/or maintenance. Expression of this factor is developmentally regulated, increasing in the brain during embryogenesis and reaching its maximum expression at the time of birth. The gene codes for a 168-residue protein that is a precursor for a previously described brain-derived heparin-binding protein of 136 amino acids

General function Ligand, Growth factor
Comment
Cellular localization Secreted
Comment
Ovarian function
Comment Nakanishi T, et al 1997 reported that pleiotropin gene was expressed in six normal ovaries and in 24 tumors (nine benign, two borderline, and 13 malignant tumors).
Expression regulated by
Comment
Ovarian localization , Follicular Fluid
Comment Ohyama Y, et al 2000 reported the isolation and identification of midkine and pleiotrophin in bovine follicular fluid. Two distinct heparin-binding polypeptides were isolated from bovine follicular fluid by successive chromatographies. N-Terminal and tryptic peptide fragment analysis of these polypeptides revealed that they are identical to midkine (MK) and pleiotrophin (PTN), respectively, which form a new family of heparin-binding growth/differentiation factors.
Follicle stages
Comment
Phenotypes
Mutations 1 mutations

Species: mouse
Mutation name: None
type: null mutation
fertility: subfertile
Comment: Female infertility in mice deficient in midkine and pleiotrophin, which form a distinct family of growth factors. Muramatsu H et al. Midkine and pleiotrophin form a family of growth factors. Mice deficient in one of the genes show few abnormalities on reproduction and development. To understand their roles in these processes, we produced mice deficient in both genes; the double deficient mice were born in only one third the number expected by Mendelian segregation and 4 weeks after birth weighed about half as much as wild-type mice. Most of the female double deficient mice were infertile. In these mice, the numbers of mature follicles and of ova at ovulation were reduced compared to numbers in wild-type mice. Both midkine and pleiotrophin were expressed in the follicular epithelium and granulosa cells of the ovary. The expression of these factors in the uterus was dramatically altered during the estrous cycle. The diestrus and proestrus periods were long and the estrus period was short in the double deficient mice, indicating the role of the factors in the estrous cycle. Furthermore, vaginal abnormality was found in about half of the double deficient mice. These abnormalities in combination resulted in female infertility. Therefore, midkine and pleiotrophin, together with their signaling receptors, play important roles in the female reproductive system.

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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
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created: Sept. 27, 2000, midnight by: hsueh   email:
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last update: Nov. 29, 2006, 7:05 a.m. by: hsueh    email:



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