MARC details
| 000 -LEADER |
| fixed length control field |
02257nam a2200253Ia 4500 |
| 003 - CONTROL NUMBER IDENTIFIER |
| control field |
MX-MdCICY |
| 005 - DATE AND TIME OF LATEST TRANSACTION |
| control field |
20250625124715.0 |
| 040 ## - CATALOGING SOURCE |
| Transcribing agency |
CICY |
| 090 ## - LOCALLY ASSIGNED LC-TYPE CALL NUMBER (OCLC); LOCAL CALL NUMBER (RLIN) |
| Classification number (OCLC) (R) ; Classification number, CALL (RLIN) (NR) |
B-8176 |
| 008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION |
| fixed length control field |
250602s9999 xx |||||s2 |||| ||und|d |
| 245 10 - TITLE STATEMENT |
| Title |
Mitogen-activated protein kinase (MAPK)-docking sites in MAPK kinases function as tethers that are crucial for MAPK regulation in vivo |
| 490 0# - SERIES STATEMENT |
| Volume/sequential designation |
Cellular Signalling, 18(1), p.123-134, 2006 |
| 520 3# - SUMMARY, ETC. |
| Summary, etc. |
Docking sites on targets of mitogen-activated protein kinases (MAPKs)facilitate accurate and efficient substrate phosphorylation. MAPK/ ERK kinases (MEKs, or MKKs), the upstream regulators of MAPKs, also contain N-terminal MAPK-docking sites, or FD-sites_; however, the in vivo functions of MEK D-sites are incompletely understood. Here we found that the ability of constitutively-active human MEK1 and MEK2 to stimulate ERK phosphorylation and to induce the neoplastic transformation of NIH 3T3 cells required the integrity of the D-site. In addition, D-site mutants of otherwise wild-type MEK1/2 were unable to anchor unphosphorylated ERK2 in the cytoplasm. ERK activation, cytoplasmic anchoring and release were completely retained in Fswap_ mutants in which MEK2's D-site was replaced with the D-site of MEK1 or yeast Ste7. Furthermore, these abilities were significantly retained when MEK2's D-site was moved to its C-terminus, or replaced by an unrelated MAPK-binding domain taken from the Ets-1 transcription factor. We conclude that the D-sites in MEKs are crucial for the activation of their cognate MAPKs in vivo, and that their primary function is to tether their cognate MAPKs near the MEK's kinase domain. This proximity effect is sufficient to explain the contribution that the D-site interaction makes to several biologically important signaling events |
| 650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
| Topical term or geographic name entry element |
MITOGEN-ACTIVATED PROTEIN KINASES |
| 650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
| Topical term or geographic name entry element |
SIGNAL TRANSDUCTION |
| 650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
| Topical term or geographic name entry element |
PHOSPHORYLATION |
| 650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
| Topical term or geographic name entry element |
BINDING SITES |
| 650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
| Topical term or geographic name entry element |
PROTEIN BINDING |
| 700 12 - ADDED ENTRY--PERSONAL NAME |
| Personal name |
Grewal, S. |
| 700 12 - ADDED ENTRY--PERSONAL NAME |
| Personal name |
Molina, D.M. |
| 700 12 - ADDED ENTRY--PERSONAL NAME |
| Personal name |
Bardwell, L. |
| 856 40 - ELECTRONIC LOCATION AND ACCESS |
| Uniform Resource Identifier |
<a href="https://drive.google.com/file/d/18pmwQ_x38R8ZMAuEO-PhvLltpK1LcesO/view?usp=drivesdk">https://drive.google.com/file/d/18pmwQ_x38R8ZMAuEO-PhvLltpK1LcesO/view?usp=drivesdk</a> |
| Public note |
Para ver el documento ingresa a Google con tu cuenta: @cicy.edu.mx |
| 942 ## - ADDED ENTRY ELEMENTS (KOHA) |
| Source of classification or shelving scheme |
Clasificación local |
| Koha item type |
Documentos solicitados |