The S-Locus Receptor Kinase Gene in a Self-Incompatible Brassica napus Line Encodes a Functional Serine/Threonine Kinase

1992 ◽  
Vol 4 (10) ◽  
pp. 1273 ◽  
Author(s):  
Daphne R. Goring ◽  
Steven J. Rothstein
Keyword(s):  
Brassica Napus ◽  
Receptor Kinase ◽  
S Locus ◽  
Serine Threonine Kinase ◽  
Kinase Gene ◽  
Threonine Kinase ◽  
Napus Line

The FAS-activated serine/threonine kinase gene maps to canine chromosome 16

2004 ◽  
Vol 35 (6) ◽  
pp. 497-497 ◽  
Author(s):  
J. Meyer ◽  
H. Murua Escobar ◽  
S. Bartnitzke ◽  
C. Schelling ◽  
G. Dolf ◽  
...  
Keyword(s):  
Chromosome 16 ◽  
Serine Threonine Kinase ◽  
Kinase Gene ◽  
Threonine Kinase ◽  
Canine Chromosome ◽  
Gene Maps

scholarly journals Sex-specific transcripts of the Dstpk61 serine/threonine kinase gene in Drosophila melanogaster

1999 ◽  
Vol 262 (2) ◽  
pp. 456-466 ◽  
Author(s):  
Colin N. MacDougall ◽  
Dorothy Clyde ◽  
Timothy Wood ◽  
Martin Todman ◽  
Diane Harbison ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Serine Threonine Kinase ◽  
Kinase Gene ◽  
Threonine Kinase

A serine/threonine kinase gene defective in Peutz–Jeghers syndrome

Nature ◽  
10.1038/34432 ◽  
1998 ◽  
Vol 391 (6663) ◽  
pp. 184-187 ◽  
Author(s):  
Akseli Hemminki ◽  
David Markie ◽  
Ian Tomlinson ◽  
Egle Avizienyte ◽  
Stina Roth ◽  
...  
Keyword(s):  
Serine Threonine Kinase ◽  
Kinase Gene ◽  
Threonine Kinase ◽  
Peutz Jeghers Syndrome

scholarly journals Involvement of a Magnaporthe grisea Serine/Threonine Kinase Gene, MgATG1, in Appressorium Turgor and Pathogenesis

2007 ◽  
Vol 6 (6) ◽  
pp. 997-1005 ◽  
Author(s):  
Xiao-Hong Liu ◽  
Jian-Ping Lu ◽  
Lei Zhang ◽  
Bo Dong ◽  
Hang Min ◽  
...  
Keyword(s):  
Lipid Droplets ◽  
Magnaporthe Grisea ◽  
Normal Development ◽  
Normal Values ◽  
Turgor Pressure ◽  
Serine Threonine Kinase ◽  
Gene Encoding ◽  
Kinase Gene ◽  
Threonine Kinase ◽  
Delayed Initiation

ABSTRACT We isolated an MgATG1 gene encoding a serine/threonine protein kinase from the rice blast fungus Magnaporthe grisea. In the ΔMgatg1 mutant, in which the MgATG1 gene had been deleted, autophagy was blocked; the mutant also showed fewer lipid droplets in its conidia, lower turgor pressure of the appressorium, and such defects in morphogenesis as delayed initiation and slower germination of conidia. As a result of lower turgor pressure of the appressorium, the ΔMgatg1 mutant lost its ability to penetrate and infect the two host plants, namely, rice and barley. However, normal values of the parameters and infective abilities were restored on reintroducing an intact copy of the MgATG1 gene into the mutant. Autophagy is thus necessary for turnover of organic matter during the formation of conidia and appressoria and for normal development and pathogenicity in M. grisea.

scholarly journals LKB1 loss in melanoma disrupts directional migration toward extracellular matrix cues

2014 ◽  
Vol 207 (2) ◽  
pp. 299-315 ◽  
Author(s):  
Keefe T. Chan ◽  
Sreeja B. Asokan ◽  
Samantha J. King ◽  
Tao Bo ◽  
Evan S. Dubose ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Adenosine Monophosphate ◽  
Time Lapse ◽  
Serine Threonine Kinase ◽  
Directional Migration ◽  
Kinase Gene ◽  
Threonine Kinase ◽  
Melanoma Invasion ◽  
Ampk Activity ◽  
Systematic Perturbation

Somatic inactivation of the serine/threonine kinase gene STK11/LKB1/PAR-4 occurs in a variety of cancers, including ∼10% of melanoma. However, how the loss of LKB1 activity facilitates melanoma invasion and metastasis remains poorly understood. In LKB1-null cells derived from an autochthonous murine model of melanoma with activated Kras and Lkb1 loss and matched reconstituted controls, we have investigated the mechanism by which LKB1 loss increases melanoma invasive motility. Using a microfluidic gradient chamber system and time-lapse microscopy, in this paper, we uncover a new function for LKB1 as a directional migration sensor of gradients of extracellular matrix (haptotaxis) but not soluble growth factor cues (chemotaxis). Systematic perturbation of known LKB1 effectors demonstrated that this response does not require canonical adenosine monophosphate–activated protein kinase (AMPK) activity but instead requires the activity of the AMPK-related microtubule affinity-regulating kinase (MARK)/PAR-1 family kinases. Inhibition of the LKB1–MARK pathway facilitated invasive motility, suggesting that loss of the ability to sense inhibitory matrix cues may promote melanoma invasion.

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