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1                                              Kirsten-Ras (K-Ras) knockout fibroblasts express undetec
2 s in codons 248 and 273 of TP53 and codon 12 Kirsten-ras (KRAS) are commonly found in human carcinoma
3 fic TM isoforms in transformed cells using a Kirsten virus-transformed cell line (ATCC NRK1569) as a
4 red with those expressing G35 to A activated Kirsten ras.
5  epidermal growth factor receptor (EGFR) and Kirsten ras (KRAS) confer sensitivity and resistance, re
6 over-expression of both wild-type Harvey and Kirsten Ras proteins as contributors to rat mammary carc
7             Oncogenic mutations in B-Raf and Kirsten-Ras (K-Ras) are mutually exclusive during human
8 s not present in human neutrophils, but both Kirsten-ras (K-ras) and Neuronal-ras are.
9              Elevated expression of either c-Kirsten A-Ras or c-Kirsten B-Ras did not reverse the apo
10 ed expression of either c-Kirsten A-Ras or c-Kirsten B-Ras did not reverse the apoptotic sensitivity
11                     We additionally compared Kirsten rat sarcoma viral oncogene homolog (KRAS) mutati
12  Exclusive activation of either the Harvey-, Kirsten-, or N-ras gene is often found in human and rode
13 1 (lung adenoma susceptibility 1) and Kras2 (Kirsten rat sarcoma oncogene 2) genes as primary candida
14 n 0.5 Mb in which at least two genes, Kras2 (Kirsten rat sarcoma oncogene 2) and Casc1 (cancer suscep
15 nesylation and carboxymethylation of KRAS4b (Kirsten rat sarcoma isoform 4b) are essential for its in
16 dermal growth factor receptor (EGFR), mutant Kirsten rat sarcoma viral oncogene homolog (Kras), or ov
17                                     Notably, Kirsten rat sarcoma (KRAS)-driven tumors have been repor
18                                Expression of Kirsten rat sarcoma viral oncogene [Kras(G12V)] and disr
19 ene derivatives bind to transient pockets on Kirsten-Ras (K-Ras) and inhibit GDP-GTP exchange.
20 lung cancer based on activation of oncogenic Kirsten rat sarcoma viral oncogene homolog (Kras) and lo
21         Aberrant expression of the oncogenic Kirsten-Ras (Ki-Ras) and interferon-stimulated gene 15 (
22 e activated or wild-type forms of Harvey- or Kirsten-ras.
23                                       K-Ras (Kirsten-rat sarcoma viral oncogene homolog) is a promine
24      Of the three different isoforms of Ras (Kirsten, Harvey, and Neural), we previously demonstrated
25 noma (PDAC) involves activation of c-Ki-ras2 Kirsten rat sarcoma oncogene homolog (KRAS) signaling, b
26                               The vi-Ki-ras2 Kirsten rat sarcoma viral oncogene (KRAS) represents one
27       Directly targeting oncogenic V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (K-Ras) with
28 se (ALK), EGF receptor (EGFR), and V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) are ma
29 imaging to provide a signature for V-KI-RAS2 Kirsten rat sarcoma viral oncogene homolog (KRAS) gene m
30           Additional activation of v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) networ
31  viral oncogene homolog B1 (BRAF), v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS), or ep
32 kers were associated with non-pCR; v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog mutation (P =
33 h both tumor protein p53 (p53) and v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog mutations had
34 her, in patients with both p53 and v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog mutations or
35 ey ras expression was 1.5-2-fold higher than Kirsten ras or N-ras at each adult stage of development,
36                  Activating mutations in the Kirsten rat sarcoma viral oncogene homolog (KRAS) underl
37                             Mutations in the Kirsten-ras (K-ras) oncogene occur early and frequently
38 th colorectal liver metastases (CRLM) is the Kirsten rat sarcoma viral oncogene homolog (KRAS); howev
39 carrying either three or seven copies of the Kirsten ras gene under the same promoter (HrKr) were pro
40 er a (Clec9a) locus causes expression of the Kirsten rat sarcoma viral oncogene homolog (Kras)(G12D)
41 Neural), we previously demonstrated that the Kirsten isoform is key in the control of renal fibroblas
42                       To examine whether the Kirsten rat sarcoma viral oncogene homolog (KRAS)-varian
43 survival disadvantage, especially within the Kirsten rat sarcoma viral oncogene homolog (KRAS) mutant
44 orexin receptor 1 (HcrtR1/OX(1)R) but not to Kirsten murine sarcoma virus transformed rat kidney epit
45 sing wild-type Harvey ras, but not wild-type Kirsten ras.
46 nitumumab on cell lines expressing wild-type Kirsten-Ras (K-Ras) and oncogenic K-Ras mutations.
47 ostate epithelial cells transformed by viral Kirsten-ras (267B1/Ki-ras cells) compared with those in
48 erall survival was found among patients with Kirsten rat sarcoma viral oncogene homolog (KRAS)-mutate

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