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1 es the regulation of alternative splicing by CELF proteins.
2 o antagonistic factor families, the MBNL and CELF proteins.
3 tive exons, both of which are antagonized by CELF proteins.
4 UNC-75, the C. elegans homolog of vertebrate CELF proteins.
5  important to identify downstream targets of CELF proteins.
6                                 The MBNL and CELF proteins act antagonistically to control the altern
7                             We conclude that CELF protein activity is required for normal alternative
8                                 We show that CELF proteins are down-regulated >10-fold during heart d
9                CUG-BP and ETR-3 like factor (CELF) proteins are regulators of pre-mRNA alternative sp
10 nding and splicing analyses demonstrate that CELF proteins block splicing through interfering with bi
11 ctive RNA processing due to misexpression of CELF proteins causes wide-reaching structural defects an
12                Like the previously described CELF proteins, CELF6 shares a domain structure containin
13                                              CELF proteins contain two adjacent RNA binding domains (
14 rich (SR) proteins SRp20 and SF2/ASF and the CELF protein CUG-BP1.
15  the two motifs were responsive to two other CELF proteins (CUG-BP1 and CELF4), indicating that diffe
16 is analysis was performed in parallel on two CELF proteins, ETR-3 (CUG-BP2, NAPOR, BRUNOL3) and CELF4
17  CUGBP2, the 2 CUGBP1 and ETR-3 like factor (CELF) proteins expressed in heart, demonstrated elevated
18 Members of the CUG-BP and ETR-3 like factor (CELF) protein family bind within conserved intronic elem
19                   This family, which we call CELF proteins for CUG-BP- and ETR-3-like factors, specif
20                        The expression of two CELF proteins is highly restricted to brain.
21          To fully understand the function of CELF proteins, it is important to identify downstream ta
22 s type I (NF1) exon 23a is a novel target of CELF protein-mediated splicing regulation in neuron-like
23                      We propose that Fox and CELF proteins play major roles in enforcing the muscle-s
24 n of different splicing events by individual CELF proteins requires separable regions, implying the n
25 ith mice overexpressing CUG-BP1, a wild-type CELF protein, rescues defects in alternative splicing, t
26 upregulation of nPTB, Tra2beta, muscleblind, CELF proteins, Sam68 and T-STAR.
27 ice that express a nuclear dominant-negative CELF protein specifically in the heart (MHC-CELFDelta) d
28                              Five of the six CELF proteins strongly suppress the inclusion of NF1 exo
29 runcation mutants to identify the regions of CELF proteins that are required to activate and to repre
30 lts place CELF6 in a functional subfamily of CELF proteins that includes CELFs 3, 4, and 5.
31 n-regulation of CUGBP and ETR-3-like factor (CELF) proteins that regulate nearly half of developmenta
32 ia expression of a nuclear dominant negative CELF protein under an alpha-myosin heavy chain promoter.
33 tive cTNT and IR exons are also regulated by CELF proteins, which were previously implicated in DM pa