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ALPHA-FETOPROTEIN; AFP OKDB#: 1672
 Symbols: ALPHA-FETOPROTEIN; AFP Species: human
 Synonyms: ALPHA-FETOPROTEIN, HEREDITARY PERSISTENCE OF, INCLUDED, HPAFP, INCLUDED| AFP DEFICIENCY, INCLUDED|  Locus: 4q11-q13 in Homo sapiens


For retrieval of Nucleotide and Amino Acid sequences please go to: OMIM Entrez Gene
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General Comment Alpha-fetoprotein is a major plasma protein in the fetus, where it is produced by the yolk sac and liver. In the adult its concentration is very low except when a tumor such as hepatoma or teratoma is present. The similarity in physical properties of AFP and albumin (103600) and the fact that their presence is inversely related suggested that AFP is the fetal counterpart of serum albumin.

NCBI Summary: This gene encodes alpha-fetoprotein, a major plasma protein produced by the yolk sac and the liver during fetal life. Alpha-fetoprotein expression in adults is often associated with hepatoma or teratoma. However, hereditary persistance of alpha-fetoprotein may also be found in individuals with no obvious pathology. The protein is thought to be the fetal counterpart of serum albumin, and the alpha-fetoprotein and albumin genes are present in tandem in the same transcriptional orientation on chromosome 4. Alpha-fetoprotein is found in monomeric as well as dimeric and trimeric forms, and binds copper, nickel, fatty acids and bilirubin. The level of alpha-fetoprotein in amniotic fluid is used to measure renal loss of protein to screen for spina bifida and anencephaly.
General function Extracellular binding protein
Comment
Cellular localization Secreted
Comment
Ovarian function Germ cell development
Comment Four cases of immature teratoma of the ovary are presented and the recent literature is reviewed by Gallion H, et al . The majority of these tumors were confined to one ovary at the time of diagnosis, and more than 75% occurred in women under 25 years of age. The two most important prognostic parameters were stage of disease and histologic grade. Optimal survival occurred when surgical tumor debulking was followed by combination chemotherapy. The addition of hysterectomy with contralateral adnexectomy did not improve the survival of patients with disease confined to one ovary. Similarly, postoperative radiation therapy was not shown to be beneficial in patients with this disease. Analysis of presently available data suggests that patients with teratocarcinoma of the ovary should be treated with tumor excision followed by at least 12 courses of chemotherapy with vincristine, actinomycin D, and cyclophosphamide. alpha-Fetoprotein may be useful as a biochemical marker of disease status in selected patients.
Expression regulated by
Comment
Ovarian localization Primordial Germ Cell
Comment Wu J, et al 2002 reported the expression of Fas, p53 and AFP in development of human fetal germ cells in vitro. A two-step culture system was used to study the expression of Fas, p53 and alpha-fetoprotein (AFP) in the development in vitro of human fetal germ cells. p53 mRNA was determined by Northern blotting, and Fas content was assessed by western blotting. RT-nested polymerase chain reaction (RT-nPCR) analysis was performed to determine the expression of AFP mRNA in different stages of fetal follicular development. Follicular cell apoptosis was evaluated by DNA fragmentation analyses (DNA ladder). The results showed that by day 7 of culture approximately one-sixth of fetal germ cells grew to class C oocytes (primary oocytes) from class B oocytes (primordial oocytes) or class A oocytes. On day 45 of culture, one-third of these primary follicles doubled in size. In the meantime, there was a high proportion apoptosis of follicular cells on days 35 or 45 of culture, as evident by a clear ladder pattern of DNA fragmentation upon electrophoretic analysis. Expression of Fas antigen and p53 mRNA increased in a time-dependent manner, while AFP mRNA was expressed on days 10 to 35, and disappeared on day 45. These results indicate that human fetal germ cells can develop in a two-step culture system and AFP may play an active role in the proliferation of these germ cells. At the late stage of follicular development in vitro a number of follicular cells became apoptotic. Moreover, apoptosis may be the mechanism responsible for fetal germ cell regression and the Fas antigen and/or p53-mediate death pathway may be central in the induction of germ cell regression.
Follicle stages
Comment
Phenotypes
Mutations 0 mutations
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created: Dec. 17, 2002, 8:15 a.m. by: hsueh   email:
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last update: Jan. 22, 2015, 2:27 p.m. by: hsueh    email:



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