Wyniki wyszukiwania

1

Implications of kinase similarity in drug discovery

100%

Vieth M., Sutherland J.

Cellular and Molecular Biology Letters

|

2005

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tom 10

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nr Suppl.2

2

Development of specific Rho-kinase inhibitor and its clinical application

100%

Tamura M., Hidaka H.

Cellular and Molecular Biology Letters

|

2005

|

tom 10

|

nr Suppl.2

3

Manipulation of alternative splicing by specific inhibitors of SR protein kinases

88%

Hagiwara M.

Cellular and Molecular Biology Letters

|

2005

|

tom 10

|

nr Suppl.2

4

P38 MAP kinase inhibitors - mechanisms and therapeutic potentials

88%

Lee J. C.

Cellular and Molecular Biology Letters

|

1998

|

tom 03

|

nr 3

5

Exploiting structural principles to generate protein kinase inhibitors

88%

Noble M., Barrett P., Endicott J., Johnson L., McDonnell J., Pratt D., Robertson G.

Cellular and Molecular Biology Letters

|

2005

|

tom 10

|

nr Suppl.2

6

Scanning the proteome for targets of kinase inhibitors using bi-functional receptor ligands

75%

Kley N.

Cellular and Molecular Biology Letters

|

2005

|

tom 10

|

nr Suppl.2

7

Strategies toward identification of novel and selective protein kinase inhibitors

75%

Traxler P., Bold G., Buchdunger E., Capraro H. G., Collingwood S., Fabbro D., Furet P., Geiger T., Imbach P., Mett H., Meyer T., Ruetz S., Zimmermann J.

Cellular and Molecular Biology Letters

|

1998

|

tom 03

|

nr 3

8

Combining medicinal chemistry with chemogenomic and computer-aided structure-based design in development of novel kinase inhibitors

75%

Vieth M., Brooks H. B., Hamdouchi C., McMillen W., Sawyer J. S., Yingling J. M., Zhang F.

Cellular and Molecular Biology Letters

|

2003

|

tom 08

|

nr 2A

9

Dasatinib treatment can overcome imatinib and nilotinib resistance in CML patient carrying F3591 mutation of BCR-ABL oncogene

63%

Baranska M., Lewandowski K., Gniot M., Iwola M., Lewandowska M., Komarnicki M.

Journal of Applied Genetics

|

2008

|

tom 49

|

nr 2

201-203

Point mutations of bcr-abl tyrosine kinase are the most frequent causes of imatinib resistance in chronic myeloid leukaemia (CML) patients. In most CML cases with BCR-ABL mutations leading to imatinib resistance the second generation of tyrosine kinase inhibitors (TKI- e.g. nilotinib or dasatinib) may be effective. Here, we report a case of a CML patient who during imatinib treatment did not obtain clinical and cytogenetic response within 12 months of therapy. The sequencing of BCR-ABL kinase domains was performed and revealed the presence of a F359I point mutation (TTC-to-ATC nucleotide change leading to Phe-to-Ile amino acid substitution). After 1 month of nilotinib therapy a rapid progression of clinical symptoms was observed. In the presence of the F359I point mutation only dasatinib treatment overcame imatinib and nilotinib resistance.

10

Efficient characterization of kinase inhibitors using LeadCodeTM technology

63%

Degenhart C.

Cellular and Molecular Biology Letters

|

2003

|

tom 08

|

nr 2A

11

Domain truncation, point mutation, and surrogation for structure based kinase inhibitor design

63%

Breitenlechner C. B., Huber R., Bossemeyer D., Gassel M., Masjost B., Engh R. A.

Cellular and Molecular Biology Letters

|

2005

|

tom 10

|

nr Suppl.2

12

Advances in the structural biology, design and clinical development of Bcr-Abl kinase inhibitors for the treatment of chronic myelogenous leukemia

63%

Manley P. W., Cowan-Jacob S., Mestan J.

Cellular and Molecular Biology Letters

|

2005

|

tom 10

|

nr Suppl.2

13

Insights into selectivity of STI571 [GleevecTM] from X-ray crystallography

63%

Nowakowski J., Sridhar V., Thompson D. A., Cronin C. N., Vaughn D. E., Gangloff A. R., Sang B. C., Zoa H., Knuth M. W., Swanson R. V., Snell G., Mol C. D., Wilson K. P., Mcree D. E.

Cellular and Molecular Biology Letters

|

2003

|

tom 08

|

nr 2A

14

KID, an interactive kinase inhibitor database

51%

Collin O., Legoff M., Meijer L.

Cellular and Molecular Biology Letters

|

1998

|

tom 03

|

nr 3

15

The formation of ceramide from sphingomyelin is associated with cellular apoptosis

51%

Dawson G., Goswami R., Kilkus J., Wiesner D.

Acta Biochimica Polonica

|

1998

|

tom 45

|

nr 2

The apoptotic response of the immature B-cell to the cross-linking of surface IgM receptors provides a good model for cell death and we show in WEHI-231 B-cells that the time course of apoptosis corresponds to the increased formation of ceramide, as measured either by mass (using the diacylglycerol kinase method) or radiolabelling with [3H]palmitate. Inhibitors of sphingosine biosynthesis have no effect on cell death induced by anti-IgM in WEHI-231 but inhibitors of ceramidase accelerate apoptosis, suggesting that activation of sphingomyelinase is the key event in apoptosis. We have demonstrated this by in vitro assay of neutral sphingomyelinase. Apoptosis is also important in normal brain development and neuronal survival is dependent upon phosphatidylinositol 3-kinase (PI3-kinase) activation by growth factors (insulin, nerve growth factor etc.). Withdrawal of these growth factors or inhibition of PI3-kinase with wortmannin or LY294002 activated the pro-apoptotic CPP32 (Yama/Apopain/caspase 3, EC 3.4.22), activated neutral sphingomyelinase and increased ceramide formation in an immortalized dorsal root ganglion cell line F-11. Protection against apoptosis can be achieved by overexpression of the bcl2 family of proteins or addition of drugs which elevate cAMP levels. cAMP protects against apoptosis induced by either wortmannin or staurosporine. The specificity for cAMP was confirmed by showing protection with the specific agonist (Sp)cAMPS and increased killing with the antagonist (Rp)cAMPS. However, cAMP did not protect against ceramide killing, suggesting that there are at least two major pathways of apoptosis in neuronal cells.

16

The P. falciparum CDK family: structural studies and implications for inhibitor design

51%

Merckx A., Zawaira A., Holton S., Doerig C., Noble M., Endicott J.

Cellular and Molecular Biology Letters

|

2005

|

tom 10

|

nr Suppl.2

17

The PI3K kinase inhibitor, LY294002, decreases rantes-induced peritoneal recruitment of neutrophils in mice

51%

Ferrandi C., Ji H., Rommel C., Cirillo R.

Cellular and Molecular Biology Letters

|

2003

|

tom 08

|

nr 2A

Ograniczanie wyników

Implications of kinase similarity in drug discovery

Development of specific Rho-kinase inhibitor and its clinical application

Manipulation of alternative splicing by specific inhibitors of SR protein kinases

P38 MAP kinase inhibitors - mechanisms and therapeutic potentials

Exploiting structural principles to generate protein kinase inhibitors

Scanning the proteome for targets of kinase inhibitors using bi-functional receptor ligands

Strategies toward identification of novel and selective protein kinase inhibitors

Combining medicinal chemistry with chemogenomic and computer-aided structure-based design in development of novel kinase inhibitors

Dasatinib treatment can overcome imatinib and nilotinib resistance in CML patient carrying F3591 mutation of BCR-ABL oncogene

Efficient characterization of kinase inhibitors using LeadCodeTM technology

Domain truncation, point mutation, and surrogation for structure based kinase inhibitor design

Advances in the structural biology, design and clinical development of Bcr-Abl kinase inhibitors for the treatment of chronic myelogenous leukemia

Insights into selectivity of STI571 [GleevecTM] from X-ray crystallography

KID, an interactive kinase inhibitor database

The formation of ceramide from sphingomyelin is associated with cellular apoptosis

The P. falciparum CDK family: structural studies and implications for inhibitor design

The PI3K kinase inhibitor, LY294002, decreases rantes-induced peritoneal recruitment of neutrophils in mice