Interference No. 104,436 Paper 98
Shyarnala v. HUIman Page 13
[971 Raingeaud notes that p38 is part of one of several signaling pathways that are activated in
response to cytokines and environmental stress, which makes isolating the function of p38
difficult [ 1009 at 1247:R].
[98] Raingeaud confirmed that MKK3 appears to activate p38 selectively, but could not rule out the
possibility that other kinases are also involved [ 1009 at 1249:R- 1250:L].
[99] Raingeaud cautioned that experimental overexpression of p38 could result in p38 MAP kinase
phosphoryIation of proteins that are not ordinarily substrates for p38 [1009 at 1250:L].
[1001 Raingeaud also confirmed that MKK6 appears to activate p38 selectively [1009 at 1252].
Diagnostic and theEgp-eutic utilities
[101] Shyamala points to the following disclosure of diagnostic and therapeutic utilities in its
provisional applications to establish utility C 1029 at 4: 1 -101:
Still another embodiment is a method of diagnosis of a disease in a patient
characterizable by aberrant MIP polypeptide mediated activity including one
selected from the group consisting of MKK3 associated activity and GTP
mediated cellular response by providing a MIP antibody, contacting a patient
tissue sample with the antibody, and detecting the amount of the MIP polypeptide
present.
Another embodiment of the invention is a method of treating a disease in a
patient characterizable by aberrant MEP polypeptide mediated activity including
one selected from the group consisting of MKK3 associated activity and GTP
mediated cellular response by providing inhibitor MIP, and administering to the
patient a sufficient amount of the inhibitor to effect a reduction in MIP
polypeptide mediated signaling within a population of cells.
[102] Shyamala elaborated on these methods later in the provisional applications [1029 at 33:9-26]:
MIP may be useful in a diagnostic context for identifying overexpression
of MIP by identifying MIP transcript in brain or spleen tissues, in the presence of
a condition characterized by abnormal activation of the p38 MAPK stress signal
transduction pathway. Additionally, genetic information of MIP may be useful for
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