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TYRO3 protein tyrosine kinase OKDB#: 2186
 Symbols: TYRO3 Species: human
 Synonyms: BYK, Dtk, RSE, Rek, Sky, Tif, Etk-2  Locus: 15q15 in Homo sapiens
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General Comment NCBI Summary: The gene is part of a 3-member transmembrane receptor kinase receptor family with a processed pseudogene distal on chromosome 15. The encoded protein is activated by the products of the growth arrest-specific gene 6 and protein S genes and is involved in controlling cell survival and proliferation, spermatogenesis, immunoregulation and phagocytosis. The encoded protein has also been identified as a cell entry factor for Ebola and Marburg viruses. [provided by RefSeq, May 2010]
General function Receptor
Comment
Cellular localization Plasma membrane
Comment
Ovarian function
Comment
Expression regulated by
Comment
Ovarian localization Primordial Germ Cell, Granulosa
Comment Matsubara N, et al. (Dev Biol. 1996) found that Sky is expressed in both primordial germ cells (PGCs) and their supporting cells in male genital ridges after 11.5 dpc. Interestingly, Sky expression was not detected in female genital ridges, although transcripts were detected in supporting cells in the developing ovary at later stages. This gene was also found in a mouse DNA array analysis of transcripts expressed in mouse preovulatory follicles.
Follicle stages Antral
Comment Global gene expression in granulosa cells of growing, plateau and atretic dominant follicles in cattle. Girard A et al. (2015) The physiological state of the dominant follicle is important as it may be linked to the competence of the oocyte within. The objective of this study was to analyze, by transcriptomic analysis, the changes occurring in granulosa cells from dominant follicles at different phases of follicular growth. Granulosa cells were collected from slaughterhouse dairy cattle follicles with a diameter greater than 9 mm, and were classified at different phases of follicle growth based on flow cytometry profiles of DNA content after staining with propidium iodide. Three phases were identified based on the proportion of cells in -G1 (less than 2n DNA), G0-G1 (2n DNA) or S-M (more than 2n DNA) and follicles were thus allocated to the growing, plateau or atresia group. Between group analysis (BGA) showed clear segregation of the three groups, and the groups were contrasted against each other in a loop design to identify differently expressed genes. Ingenuity Pathway Analysis (IPA) was used to identify the functions and upstream regulators associated with the observed differently expressed genes. Major differences were observed between the growth phases. Granulosa cells from follicles in the plateau phase had increased expression of TYRO3 and downregulation of JAM2 compared to growing follicles, supporting the idea of a shift from proliferation to differentiation. On the other hand, genes regulating the response to oxidative stress (VNN1) and angiogenesis (ANGPT2) were upregulated in granulosa cells from atretic follicles. While the predicted activated functions in cells at the plateau stage compared to cells at the growing stage included synthesis and transport of molecules, the predictions for atretic follicles relative to plateau ones included an increase in apoptosis and cell death. Consistent with previous studies, these observations allowed us to match the presence of specific gene transcripts to a particular physiological status and consequently to classify follicles. The results also demonstrated that the plateau phase is not a simple 'in between' status between growth and atresia, as several characteristics are unique to this stage.//////////////////
Phenotypes
Mutations 1 mutations

Species: mouse
Mutation name: None
type: null mutation
fertility: infertile - non-ovarian defect
Comment: Hypothalamic but not pituitary or ovarian defects underlie the reproductive abnormalities in Axl/Tyro3 null mice. Pierce A et al. AXL and TYRO3, members of the TYRO3, AXL and MER (TAM) family of tyrosine kinase receptors, modulate GnRH neuronal cell migration, survival and gene expression. Axl/Tyro3 null mice exhibit a selective loss of GnRH neurons, delayed sexual maturation and irregular estrous cycles. Here we determined whether the defects were due to direct ovarian defects, altered pituitary sensitivity to GnRH and/or an impaired LH surge mechanism. Ovarian histology and markers of folliculogenesis and atresia as well as corpora luteal development and ovarian response to superovulation were not impaired. Axl/Tryo3 null mice exhibited a robust LH response to exogenous GnRH, suggesting no altered pituitary sensitivity. Ovariectomized Axl/Tyro3 null mice, however, demonstrated an impaired ability to mount a steroid-induced LH surge. Loss of GnRH neurons in Axl/Tyro3 null mice impairs the sex hormone-induced gonadotropin surge resulting in estrous cycle abnormalities confirming that TAM family members contribute to normal female reproductive function.

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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.)
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created: Oct. 14, 2003, 10:40 a.m. by: xin   email:
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last update: May 1, 2015, 9:45 a.m. by: hsueh    email:



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