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Journal articles on the topic 'STEP'

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Published: 4 June 2021
Last updated: 8 June 2024

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1

David, Rachel. "SteC actin rearrangements, step by step." Nature Reviews Microbiology 11, no. 1 (December 3, 2012): 5. http://dx.doi.org/10.1038/nrmicro2936.

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2

Hasson, M. S., D. Blinder, J. Thorner, and D. D. Jenness. "Mutational activation of the STE5 gene product bypasses the requirement for G protein beta and gamma subunits in the yeast pheromone response pathway." Molecular and Cellular Biology 14, no. 2 (February 1994): 1054–65. http://dx.doi.org/10.1128/mcb.14.2.1054-1065.1994.

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The STE5 gene encodes an essential element of the pheromone response pathway which is known to act either after the G subunit encoded by the STE4 gene or at the same step. Mutations in STE5, designated STE5Hyp, that partially activate the pathway in the absence of pheromone were isolated. One allele (STE5Hyp-2) was shown to cause a single amino acid substitution near the N terminus of the predicted STE5 protein. Immunoblotting with anti-Ste5 antibodies indicated that the phenotype was not due to an increased level of the mutant STE5 protein. A multicopy episomal plasmid containing a STE5Hyp allele partially suppressed both the block in pheromone-inducible transcription and the sterility phenotype caused by null alleles of the STE2, STE4, or STE18 gene, indicating that the STE5 product acts after the receptor (STE2 product) and after the G protein beta and gamma subunits (STE4 and STE18 products, respectively). However, the phenotypes of the STE5Hyp mutations were less pronounced in ste4 and ste18 mutants, suggesting that the STE5Hyp-generated signal partially depends on the proposed G beta gamma complex. The STE5Hyp alleles did not suppress ste7, ste11, ste12, or fus3 kss1 null mutants, consistent with previous findings that the STE5 product acts before the protein kinases encoded by STE7, STE11, FUS3, and KSS1 and the transcription factor encoded by STE12. The mating defects of the ste2 deletion mutant and the temperature-sensitive ste4-3 mutant were also suppressed by overexpression of wild-type STE5. The slow-growth phenotype manifested by cells carrying STE5Hyp alleles was enhanced by the sst2-1 mutation; this effect was eliminated in ste4 mutants. These results provide the first evidence that the STE5 gene product performs its function after the G protein subunits.
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3

Hasson, M. S., D. Blinder, J. Thorner, and D. D. Jenness. "Mutational activation of the STE5 gene product bypasses the requirement for G protein beta and gamma subunits in the yeast pheromone response pathway." Molecular and Cellular Biology 14, no. 2 (February 1994): 1054–65. http://dx.doi.org/10.1128/mcb.14.2.1054.

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The STE5 gene encodes an essential element of the pheromone response pathway which is known to act either after the G subunit encoded by the STE4 gene or at the same step. Mutations in STE5, designated STE5Hyp, that partially activate the pathway in the absence of pheromone were isolated. One allele (STE5Hyp-2) was shown to cause a single amino acid substitution near the N terminus of the predicted STE5 protein. Immunoblotting with anti-Ste5 antibodies indicated that the phenotype was not due to an increased level of the mutant STE5 protein. A multicopy episomal plasmid containing a STE5Hyp allele partially suppressed both the block in pheromone-inducible transcription and the sterility phenotype caused by null alleles of the STE2, STE4, or STE18 gene, indicating that the STE5 product acts after the receptor (STE2 product) and after the G protein beta and gamma subunits (STE4 and STE18 products, respectively). However, the phenotypes of the STE5Hyp mutations were less pronounced in ste4 and ste18 mutants, suggesting that the STE5Hyp-generated signal partially depends on the proposed G beta gamma complex. The STE5Hyp alleles did not suppress ste7, ste11, ste12, or fus3 kss1 null mutants, consistent with previous findings that the STE5 product acts before the protein kinases encoded by STE7, STE11, FUS3, and KSS1 and the transcription factor encoded by STE12. The mating defects of the ste2 deletion mutant and the temperature-sensitive ste4-3 mutant were also suppressed by overexpression of wild-type STE5. The slow-growth phenotype manifested by cells carrying STE5Hyp alleles was enhanced by the sst2-1 mutation; this effect was eliminated in ste4 mutants. These results provide the first evidence that the STE5 gene product performs its function after the G protein subunits.
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4

GICQUEL, J., and HS DUA. "Step by step limbal stem cell transplantation techniques." Acta Ophthalmologica 91 (August 2013): 0. http://dx.doi.org/10.1111/j.1755-3768.2013.2631.x.

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5

Jenness, D. D., B. S. Goldman, and L. H. Hartwell. "Saccharomyces cerevisiae mutants unresponsive to alpha-factor pheromone: alpha-factor binding and extragenic suppression." Molecular and Cellular Biology 7, no. 4 (April 1987): 1311–19. http://dx.doi.org/10.1128/mcb.7.4.1311-1319.1987.

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Mutations in six genes that eliminate responsiveness of Saccharomyces cerevisiae a cells to alpha-factor were examined by assaying the binding of radioactively labeled alpha-factor to determine whether their lack of responsiveness was due to the absence of alpha-factor receptors. The ste2 mutants, known to be defective in the structural gene for the receptor, were found to lack receptors when grown at the restrictive temperature; these mutations probably affect the assembly of active receptors. Mutations in STE12 known to block STE2 mRNA accumulation also resulted in an absence of receptors. Mutations in STE4, 5, 7, and 11 partially reduced the number of binding sites, but this reduction was not sufficient to explain the loss of responsiveness; the products of these genes appear to affect postreceptor steps of the response pathway. As a second method of distinguishing the roles of the various STE genes, we examined the sterile mutants for suppression. Mating of the ste2-3 mutant was apparently limited by its sensitivity to alpha-factor, as its sterility was suppressed by mutation sst2-1, which leads to enhanced alpha-factor sensitivity. Sterility resulting from each of four ste4 mutations was suppressed partially by mutation sst2-1 or by mutation bar1-1 when one of three other mutations (ros1-1, ros2-1, or ros3-1) was also present. Sterility of the ste5-3 mutant was suppressed by mutation ros1-1 but not by sst2-1. The ste7, 11, and 12 mutations were not suppressed by ros1 or sst2. Our working model is that STE genes control the response to alpha-factor at two distinct steps. Defects at one step (requiring the STE2 gene are suppressed (directly or indirectly) by mutation sst2-1, whereas defects at the other step (requiring the STE5 gene) are suppressed by the ros1-1 mutation. The ste4 mutants are defective for both steps. Mutation ros1-1 was found to be allelic to cdc39-1. Map positions for genes STE2, STE12, ROS3, and FUR1 were determined.
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6

Jenness, D. D., B. S. Goldman, and L. H. Hartwell. "Saccharomyces cerevisiae mutants unresponsive to alpha-factor pheromone: alpha-factor binding and extragenic suppression." Molecular and Cellular Biology 7, no. 4 (April 1987): 1311–19. http://dx.doi.org/10.1128/mcb.7.4.1311.

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Mutations in six genes that eliminate responsiveness of Saccharomyces cerevisiae a cells to alpha-factor were examined by assaying the binding of radioactively labeled alpha-factor to determine whether their lack of responsiveness was due to the absence of alpha-factor receptors. The ste2 mutants, known to be defective in the structural gene for the receptor, were found to lack receptors when grown at the restrictive temperature; these mutations probably affect the assembly of active receptors. Mutations in STE12 known to block STE2 mRNA accumulation also resulted in an absence of receptors. Mutations in STE4, 5, 7, and 11 partially reduced the number of binding sites, but this reduction was not sufficient to explain the loss of responsiveness; the products of these genes appear to affect postreceptor steps of the response pathway. As a second method of distinguishing the roles of the various STE genes, we examined the sterile mutants for suppression. Mating of the ste2-3 mutant was apparently limited by its sensitivity to alpha-factor, as its sterility was suppressed by mutation sst2-1, which leads to enhanced alpha-factor sensitivity. Sterility resulting from each of four ste4 mutations was suppressed partially by mutation sst2-1 or by mutation bar1-1 when one of three other mutations (ros1-1, ros2-1, or ros3-1) was also present. Sterility of the ste5-3 mutant was suppressed by mutation ros1-1 but not by sst2-1. The ste7, 11, and 12 mutations were not suppressed by ros1 or sst2. Our working model is that STE genes control the response to alpha-factor at two distinct steps. Defects at one step (requiring the STE2 gene are suppressed (directly or indirectly) by mutation sst2-1, whereas defects at the other step (requiring the STE5 gene) are suppressed by the ros1-1 mutation. The ste4 mutants are defective for both steps. Mutation ros1-1 was found to be allelic to cdc39-1. Map positions for genes STE2, STE12, ROS3, and FUR1 were determined.
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7

Douay, Luc. "Hematopoietic Stem Cell Protocols: Hematopoietic stem cell analysis ‘step by step’." Trends in Immunology 23, no. 9 (September 2002): 464. http://dx.doi.org/10.1016/s1471-4906(02)02271-8.

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8

Velardi, Andrea. "Haploidentical Hematopoietic Stem Cell Transplantation: Step-by-Step Progress." Biology of Blood and Marrow Transplantation 21, no. 4 (April 2015): 579–80. http://dx.doi.org/10.1016/j.bbmt.2015.02.004.

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9

Vasilyev, A. V., Yu S. Bakhracheva, Kabore Оusman, and Yu O. Zelenskiy. "Valve Cam Design Using Numerical Step-by-Step Method." Vestnik Volgogradskogo gosudarstvennogo universiteta. Serija 10. Innovatcionnaia deiatel’nost’, no. 1 (March 2014): 26–32. http://dx.doi.org/10.15688/jvolsu10.2014.1.4.

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10

Tompers, Dennie M., and Patricia A. Labosky. "Electroporation of Murine Embryonic Stem Cells: A Step-by-Step Guide." STEM CELLS 22, no. 3 (May 2004): 243–49. http://dx.doi.org/10.1634/stemcells.22-3-243.

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11

Cross, F. R. "The DAF2-2 mutation, a dominant inhibitor of the STE4 step in the alpha-factor signaling pathway of Saccharomyces cerevisiae MAT alpha cells." Genetics 126, no. 2 (October 1, 1990): 301–8. http://dx.doi.org/10.1093/genetics/126.2.301.

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Abstract A dominant mutation (DAF2-2) resulting in resistance to the mating pheromone alpha-factor in Saccharomyces cerevisiae MATa cells was identified and characterized genetically. Whereas wild-type cells induce a high level of the FUS1 mRNA from a low baseline on exposure to alpha-factor, DAF2-2 cells were constitutive producers of an intermediate level of FUS1 RNA; the level was increased only modestly by alpha-factor. FUS1 constitutivity required STE4, STE5 and STE18, but did not require STE2, the alpha-factor receptor gene. DAF2-2 suppressed the alpha-factor supersensitivity of a STE2 C-terminal truncation, and suppressed lethality due to scg1 mutations. Thus DAF2-2 may act by uncoupling the signaling pathway from alpha-factor binding at some point in the pathway between Scg1 inactivation and the action of Ste4, Ste5 and Ste18; this uncoupling might occur at the expense of partial constitutive activation of the pathway. DAF2-2 suppressed the unconditional cell-cycle arrest phenotype of a dominant "constitutive signaling" allele of STE4 (STE4Hpl), although the constitutive FUS1 phenotype of DAF2-2 was suppressed by ste4 null mutations; therefore DAF2-2 may directly affect the performance of the STE4 step.
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12

Soveral Martins, Alexandre de. "One step behind." Revista Electrónica de Direito 22, no. 2 (June 2020): 118–25. http://dx.doi.org/10.24840/2182-9845_2020-0002_0006.

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It is possible to plan power transition in family companies. That may be the best way of choosing the most prepared to continue the business, and it will allow a softer transition in order to avoid unnecessary value destruction. This article focuses on some of the tools that Portuguese Company Law provides to achieve those goals.
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13

SHAHED, Syed Mohammad Fakruddin. "Step into Nanoworld." Hyomen Kagaku 37, no. 1 (2016): 41–42. http://dx.doi.org/10.1380/jsssj.37.41.

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14

Light, Timothy, Gwen T. Wang, and Carol Pan Chen. "Chinese Step-by-Step, Step One." Modern Language Journal 75, no. 1 (1991): 132. http://dx.doi.org/10.2307/329852.

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15

Yang, Lucia, and Gwen T. Wang. "Chinese Step-by-Step (Step One)." Modern Language Journal 71, no. 1 (1987): 82. http://dx.doi.org/10.2307/326766.

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16

Balibar, S., C. Guthmann, and E. Rolley. "Step degeneracy and step-step interactions." Surface Science Letters 283, no. 1-3 (March 1993): A244. http://dx.doi.org/10.1016/0167-2584(93)90692-c.

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17

Balibar, S., C. Guthmann, and E. Rolley. "Step degeneracy and step-step interactions." Surface Science 283, no. 1-3 (March 1993): 290–99. http://dx.doi.org/10.1016/0039-6028(93)90994-u.

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18

Monge, L. "Step by step." Journal of AMD 23, no. 1 (April 2020): 4. http://dx.doi.org/10.36171/jamd20.23.1.01.

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19

Jones, Mark. "Step by step." Nursing Standard 15, no. 35 (May 16, 2001): 22. http://dx.doi.org/10.7748/ns.15.35.22.s33.

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20

Dobson, John. "Step by step." Nursing Standard 15, no. 9 (November 15, 2000): 18–19. http://dx.doi.org/10.7748/ns.15.9.18.s34.

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21

Morrell, Clare. "Step by step." Nursing Standard 17, no. 24 (February 26, 2003): 24. http://dx.doi.org/10.7748/ns.17.24.24.s38.

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22

Köhler, Barbara. "Step by Step." Plant Signaling & Behavior 2, no. 4 (July 2007): 303–5. http://dx.doi.org/10.4161/psb.2.4.4068.

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23

Ermel, Johannes. "Step by Step." physiopraxis 4, no. 09 (June 21, 2012): 30–33. http://dx.doi.org/10.1055/s-0032-1308026.

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24

&NA;. "Step by Step." Pediatric Physical Therapy 24, no. 3 (2012): 217. http://dx.doi.org/10.1097/pep.0b013e31825de430.

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25

Chilian, William M., Liya Yin, and Vahagn Ohanyan. "Step by Step." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 3 (March 2020): 498–99. http://dx.doi.org/10.1161/atvbaha.120.313811.

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26

Sawalha, Amr H., Michael S. Bronze, Sanjay Saint, Steve Blevins, and William Kern. "Step by Step." New England Journal of Medicine 349, no. 23 (December 4, 2003): 2253–57. http://dx.doi.org/10.1056/nejmcps031245.

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27

Cesari, Francesca. "Step by step." Nature Reviews Molecular Cell Biology 11, no. 1 (December 9, 2009): 7. http://dx.doi.org/10.1038/nrm2824.

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28

Gagescu, Raluca. "Step by step." Nature Reviews Molecular Cell Biology 3, no. 2 (February 2002): 78. http://dx.doi.org/10.1038/nrm741.

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29

Clarkson, Sheilagh. "Step by step." Nature Reviews Microbiology 2, no. 7 (July 2004): 525. http://dx.doi.org/10.1038/nrmicro940.

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30

Marte, Barbara. "Step by step." Nature Reviews Cancer 6, S1 (April 2006): S16. http://dx.doi.org/10.1038/nrc1856.

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31

O′Herlihy, Cormac. "Step by step." Managing Service Quality: An International Journal 1, no. 3 (March 1991): 149–52. http://dx.doi.org/10.1108/eum0000000003140.

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32

Russell, Meredith Jones. "Step by step." Nursery World 2019, no. 2 (January 21, 2019): 36–37. http://dx.doi.org/10.12968/nuwa.2019.2.36.

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33

Kirkwood, Keith. "Step by Step." Civil Engineering Magazine Archive 88, no. 8 (September 2018): 64–82. http://dx.doi.org/10.1061/ciegag.0001313.

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34

Hartman, Melissa A. "Step by Step." TEACHING Exceptional Children 41, no. 6 (July 2009): 6–11. http://dx.doi.org/10.1177/004005990904100601.

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35

Ogilvie, Christine R. "Step by Step." TEACHING Exceptional Children 43, no. 6 (July 2011): 20–26. http://dx.doi.org/10.1177/004005991104300602.

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36

Brazzale, Katherine. "Step by step." BMJ 330, Suppl S6 (June 1, 2005): 0506238. http://dx.doi.org/10.1136/sbmj.0506238.

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37

Fonseca, Marcelo, Vera Lúcia Jornada Krebs, and Werther Brunow de Carvalho. "Step by step." Pediatric Critical Care Medicine 13, no. 4 (July 2012): 486–87. http://dx.doi.org/10.1097/pcc.0b013e3182417720.

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38

Taylor, Angela. "Step by Step." Journal of Drug Issues 42, no. 3 (July 2012): 279–97. http://dx.doi.org/10.1177/0022042612456018.

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39

Lohse, Jon. "Step by Step." Lithic Technology 36, no. 2 (September 2011): 97–108. http://dx.doi.org/10.1179/lit.2011.36.2.97.

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40

Rutjens, Bastiaan T., Frenk van Harreveld, and Joop van der Pligt. "Step by Step." Current Directions in Psychological Science 22, no. 3 (June 2013): 250–55. http://dx.doi.org/10.1177/0963721412469810.

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41

 . "Step by step." TandartsPraktijk 27, no. 7 (July 2006): 611. http://dx.doi.org/10.1007/bf03072888.

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42

Leuzinger-Bohleber, Marianne, Mariam Tahiri, and Nora Hettich. "STEP-BY-STEP." Psychotherapeut 62, no. 4 (July 2017): 341–47. http://dx.doi.org/10.1007/s00278-017-0208-6.

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43

Bosman, Fred. "Step by step." Virchows Archiv 464, no. 1 (January 2014): 1–2. http://dx.doi.org/10.1007/s00428-013-1530-1.

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44

Fox, Monique N. "Step by Step." Critical Perspectives on Accounting 9, no. 4 (August 1998): 433. http://dx.doi.org/10.1006/cpac.1996.0250.

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45

Swinburne, Adrian. "Step by Step." Manufacturing Management 2019, no. 5 (May 2019): 32–33. http://dx.doi.org/10.12968/s2514-9768(22)90528-9.

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46

Weickmann, Dorion. "step by step." tanz 15, no. 6 (2024): 61. http://dx.doi.org/10.5771/1869-7720-2024-6-061.

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47

Burlaienko, Tetiana, Oksana Dubinina, and Piotr Magier. "Five steps against bullying (Ukraine experience): «step by step – together to success!»." Bulletin of Postgraduate Education (Series) 24, no. 53 (2023): 24–40. http://dx.doi.org/10.58442/2218-7650-2023-24(53)-24-40.

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48

Printen, J. A., and G. F. Sprague. "Protein-protein interactions in the yeast pheromone response pathway: Ste5p interacts with all members of the MAP kinase cascade." Genetics 138, no. 3 (November 1, 1994): 609–19. http://dx.doi.org/10.1093/genetics/138.3.609.

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Abstract We have used the two-hybrid system of Fields and Song to identify protein-protein interactions that occur in the pheromone response pathway of the yeast Saccharomyces cerevisiae. Pathway components Ste4p, Ste5p, Ste7p, Ste11p, Ste12p, Ste20p, Fus3p and Kss1p were tested in all pairwise combinations. All of the interactions we detected involved at least one member of the MAP kinase cascade that is a central element of the response pathway. Ste5p, a protein of unknown biochemical function, interacted with protein kinases that operate at each step of the MAP kinase cascade, specifically with Ste11p (an MEKK), Ste7p (an MEK), and Fus3p (a MAP kinase). This finding suggests that one role of Ste5p is to serve as a scaffold to facilitate interactions among members of the kinase cascade. In this role as facilitator, Ste5p may make both signal propagation and signal attenuation more efficient. Ste5p may also help minimize cross-talk with other MAP kinase cascades and thus ensure the integrity of the pheromone response pathway. We also found that both Ste11p and Ste7p interact with Fus3p and Kss1p. Finally, we detected an interaction between one of the MAP kinases, Kss1p, and a presumptive target, the transcription factor Ste12p. We failed to detect interactions of Ste4p or Ste20p with any other component of the response pathway.
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49

Nikitina, E. S. "TECHNOLOGY STEP BY STEP AS A MEANS OF DEVELOPMENT OF YOUNGER SCHOOLCHILDREN’S COGNITIVE ACTIVITY." Pedagogical Review, no. 1 (2019): 48–58. http://dx.doi.org/10.23951/2307-6127-2019-1-48-58.

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50

Pryke, Jacqueline. "Step by step progress." Nursing Standard 19, no. 28 (March 30, 2005): 58. http://dx.doi.org/10.7748/ns.19.28.58.s58.

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