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"oncogene theory"¿¡ ´ëÇÑ °Ë»ö °á°úÀÔ´Ï´Ù. °Ë»ö °á°ú º¸´Â µµÁß¿¡ Tab ۸¦ ´©¸£½Ã¸é °Ë»ö âÀÌ ¼±Åõ˴ϴÙ.
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  • ¿µ¹®
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  • personality theory
    ÀΰÝÀÌ·Ð
  • quantum theory
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  • somatic mutation theory
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  • social learning theory
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  • template theory
    Ç×ü»ý»êÁö½Ã¼³, ÅÆÇø´¼³
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    ÇѱÛ
  • double-axis theory
    ÀÌÁßÃàÀÌ·Ð
  • enzyme trace substance theory
    È¿¼ÒÈçÀû¹°¼³
  • error theory
    Âø¿ÀÀÌ·Ð
  • factor theory
    ¿äÀÎÀÌ·Ð
  • family system theory
    °¡Á·Ã¼°è·Ð
  • functional matrix theory
    ±â´É¼º±âÁú¼³
  • gate-control theory
    ¹®Á¶ÀýÀÌ·Ð
  • general system theory
    ÀϹÝü°è·Ð
  • germ line theory
    Ç×ü³»¸²¹°·Á¹Þ±â¼³
  • hemodyamic theory
    Ç÷¾×µ¿·Â¼³
  • instinct theory
    º»´ÉÀÌ·Ð
  • instructive theory
    (¢¡template theory) Ç×ü»ý»êÁö½Ã¼³, Ç×ü»ý»êÃø¼â¼³
  • internuncial pool theory
    ½Å°æ¼¼Æ÷»çÀÌÀúÀå·Ð
  • interpersonal theory
    ´ëÀÎÀÌ·Ð
  • libido theory
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  • ¿µ¹®
    ÇѱÛ
  • instinct theory
    º»´É ÀÌ·Ð
  • instructive theory of antibody production
    Áö·É¼³ (Ç×ü»ý»ê)
  • personality structure, Jungian theory
    Àΰݱ¸Á¶
  • personality theory
    ÀΰÝÀÌ·Ð
  • place theory
    ºÎÀ§¼³(Ý»êÈæò).
  • polychromatic theory
    ´Ù»ö¼³
  • psychoanalytic theory
    Á¤½ÅºÐ¼®ÇÐÀÌ·Ð(¡­ùÊìµÖå).
  • quantum theory
    ¾çÀÚ·Ð.
  • radiation,target theory of
    ¡­ÀÇ Ç¥ÀûÀÌ·Ð(¡­øöîÜìµÖå)
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  • ¿µ¹®
    ÇѱÛ
  • clonal selection theory
    Ŭ·Ð¼±Åü³
  • clonal selection theory
    Ŭ·Ð¼±Åü³.
  • colloid theory
    ÄÝ·ÎÀ̵弳(¡­æò).
  • communication theory
    ÀÇ»ç¼ÒÅëÀÌ·Ð(ëòÞÖáÂ÷×ìµÖå)
  • conditioning theory
    Á¶°ÇÈ­ÀÌ·Ð(ðÉËìûùìµÖå)
  • contagium theory
    Àü¿°¼³(ËøËçËç), °¨¿°¼³(˧ËçËç).
  • convergence-projection theory
    ÆøÁÖ Åõ»ç¼³(ÜßñÍ÷áÞÒæò).
  • corpuscular theory
    ÀÔÀÚ¼³(í£í­æò).
  • countercurrent theory
    ¿ª·ù¼³(æ½êüæò), ´ëÇâ·ù¼³.
  • cross-linking theory
    ±³Â÷¿¬°üÀÌ·Ð(Îßó©ææÎ¼ìµÖå)
  • decathexis theory
    Å»(÷­)¸®ºñµµºÎÂø(ݾó·) ÀÌ·Ð(ìµÖå)
  • developmental balance theory
    ¹ß´ÞÆòÇü¼³(¡­øÁû¬æò).
  • developmental theory
    ¹ß´ÞÀÌ·Ð(Û¡Ó¹ìµÖå)
  • dichotomous theory
    2ºÐ¹ýÇм³.
  • direct template theory
    Á÷Á¢ÁÖÇü¼³ (¡­ñÑúþæò).
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  • ¿µ¹®
    ÇѱÛ
  • eversion theory
    ¿Ü¹øÀÌ·Ð (èâÛè×âÖå)
  • evolution theory
    ÁøÈ­·Ð(òäûùÖå)
  • exhaustion theory
    °í°¥ ÀÌ·Ð (ͽÊä×âÖå)
  • factor theory
    ÀÎÀÚ ÀÌ·Ð(ì×í­×âÖå)
  • fluctuation theory
    ¿äµ¿ ÀÌ·Ð(èôÔÑ×âÖå)
  • frozen accident theory
    »ç°í µ¿°á ÀÌ·Ð(ÞÀͺÔÐÌ¿×âÖå)
  • germ-line theory
    ¹èÀÚ°è¿­ ÀÌ·Ð(ÛÏí­Í§Öª×âÖå)
  • hit theory
    °¡°Ý ÀÌ·Ð(ʥ̪×âÖå)
  • imbalance theory
    ºÒ±ÕÇü ÀÌ·Ð(ÝÕгû¬×âÖå)
  • immune surveillance theory
    ¸é¿ª °¨½Ã ÀÌ·Ð(Øóæ¹ÊøãÊ×âÖå)
  • immunological surveillance theory
    ¸é¿ª °¨½Ã ÀÌ·Ð(Øóæ¹ÊøãÊ×âÖå)
  • inchworm theory
    ÀÚ¹ú·¹ ÀÌ·Ð(×âÖå)
  • induced fit theory
    À¯µµÀûÇÕÀÌ·Ð(ë¯Óôîêùê×âÖå)
  • information theory
    Á¤º¸·Ð(ï×ÜÃÒÕ)
  • instructive theory
    Áö½Ã¼³(ò¦ãÆàã)
KMLE ÀÇÇоà¾î »çÀü À¯»ç °Ë»ö °á°ú : 5 ÆäÀÌÁö: 2
GnRH Gonadotropin Releasing Hormone  [HP 1898, 2034]
  = LHRH
  = Go...
AXL anexelekto [oncogene]; axillary lymphoscintigraphy
c-onc cellular oncogene
ONC oncogene; oncology; Orthopaedic Nursing Certificate; over-the-needle catheter
src Rous sarcoma oncogene
KMLE ÀÚµ¿ÃßÃâ ÀÇÇоà¾î »çÀü À¯»ç °Ë»ö °á°ú : 4 ÆäÀÌÁö: 2
SDT Signal Detection Theory
TOM Theory of Mind
TPB Theory of Planned Behavior
TRA Theory of Reasoned Action
°æºÏ´ë Ä¡°ú´ëÇÐ ±¸°­³»°ú ±³½Ç »çÀü À¯»ç °Ë»ö °á°ú : 15 ÆäÀÌÁö: 2
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    ¿ÀÂ÷ ´©Àû¼³
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  • fluid mosaic theory
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  • ionic theory
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  • Jackson's theory
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    ÀηùÀÇ ³ú¼ö´Â °¡Àå »óºÎ¿¡ ÀÖÀ»¼ö·Ï ÁøÈ­ÇÑ °ÍÀÌ´Ù.
  • Kubelka-Munk theory
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  • libido theory
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  • menophylectic theory
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  • MIE theory
    MIE ¼³
  • migration theory
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  • monoclonal theory
    ´ÜÀÏ ¼¼Æ÷ À¯·¡¼³
  • oxidation theory
    »êÈ­¼³
  • polychromatic theory
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  • Prothero cone theory
    ÇÁ·Îµ¥·Î ÄÜ ¼³
  • psychological theory
    ½É¸®ÇÐ ÀÌ·Ð
CancerWEB ¿µ¿µ ÀÇÇлçÀü À¯»ç °Ë»ö °á°ú : 15 ÆäÀÌÁö: 2
proto-oncogene proteins c-mos Cellular proteins encoded by the c-mos genes (genes, mos). They function in the cell cycle to maintain maturation-promoting factor in the active state and have protein-serine/threonine kinase activity. Oncogenic transformation can take place when c-mos proteins are expressed at the wrong time.
(12 Dec 1998)
proto-oncogene proteins c-myc Cellular DNA-binding proteins encoded by the c-myc genes. They are normally involved in nucleic acid metabolism and in mediating the cellular response to growth factors. Elevated and deregulated (constitutive) expression of c-myc proteins can cause tumourigenesis.
(12 Dec 1998)
proto-oncogene proteins c-raf <enzyme> A class of serine-threonine kinases involved in cellular signal transduction. Included in this class are the proto-oncogene proteins mil and raf. Raf is a component of a signal transduction pathway leading to increased gene expression through the c-jun DNA binding site, ap1.
Registry number: EC 2.7.10.-
(12 Dec 1998)
dominant oncogene <genetics, molecular biology, oncology> A gene that stimulates cell proliferation and can drastically increase the risk of cancer development when present in a single copy.
(09 Oct 1997)
immortalising oncogene <molecular biology> A gene that upon transfectionenables a primary cell to grow indefinitely in culture.
(09 Oct 1997)
oncogene <molecular biology, oncology> Mutated and/or overexpressed version of a normal gene of animal cells (the proto-oncogene) that in a dominant fashion can release the cell from normal restraints on growth and thus alone or in concert with other changes, convert a cell into a tumour cell.
(18 Nov 1997)
oncogene protein gp140(v-fms) Transforming glycoprotein coded by the fms oncogene from the susan mcdonough strain of feline sarcoma virus (sm-fesv). The oncogene protein v-fms lacks sequences, which, in the highly homologous proto-oncogene protein c-fms (csf-1 receptor), normally serve to regulate its tyrosine kinase activity. The missing sequences in v-fms mimic the effect of ligand and lead to constitutive cell growth. The protein gp120(v-fms) is post-translationally modified to generate gp140(v-fms).
(12 Dec 1998)
oncogene protein p21(ras) Transforming protein encoded by ras oncogenes. Point mutations in the cellular ras gene (c-ras) can also result in a mutant p21 protein that can transform mammalian cells. Oncogene protein p21(ras) has been directly implicated in human neoplasms, perhaps accounting for as much as 15-20% of all human tumours.
(12 Dec 1998)
oncogene protein p55(v-myc) Transforming protein coded by myc oncogenes. The v-myc protein has been found in several replication-defective avian retrovirus isolates which induce a broad spectrum of malignancies.
(12 Dec 1998)
oncogene protein p65(gag-jun) Transforming protein coded by jun oncogenes (genes, jun). This is a gag-onc fusion protein of about 65 kD derived from avian sarcoma virus. V-jun lacks a negative regulatory domain that regulates transcription in c-jun.
(12 Dec 1998)
oncogene protein pp60(v-src) <chemical> Tyrosine-specific protein kinase encoded by the v-src oncogene of rous sarcoma virus. The transforming activity of pp60(v-src) depends on both the lack of a critical carboxy-terminal tyrosine phosphorylation site at position 527, and the attachment of pp60(v-src) to the plasma membrane which is accomplished by myristylation of its n-terminal glycine.
Chemical name: Kinase (phosphorylating), protein pp60src
(12 Dec 1998)
oncogene proteins Proteins coded by oncogenes. They include proteins resulting from the fusion of an oncogene and another gene (oncogene proteins, fusion).
(12 Dec 1998)
oncogene proteins, fusion The translation products of the fusion between an oncogene and another gene. The latter may be of viral or cellular origin.
(12 Dec 1998)
oncogene proteins v-abl Transforming proteins encoded by the abl oncogenes. Oncogenic transformation of c-abl to v-abl occurs by insertional activation that results in deletions of specific n-terminal amino acids.
(12 Dec 1998)
oncogene proteins v-erba Transforming proteins encoded by erba oncogenes from the avian erythroblastosis virus. They are truncated versions of c-erba, the thyroid hormone receptor (receptors, thyroid hormone) that have retained both the DNA-binding and hormone-binding domains. Mutations in the hormone-binding domains abolish the transcriptional activation function. V-erba acts as a dominant repressor of c-erba, inducing transformation by disinhibiting proliferation.
(12 Dec 1998)
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