Appeal No. 1999-1393
Application No. 08/242,344
GROUNDS OF REJECTION29
Claims 23, 25, 26, 37, 39, and 43-45 are rejected under 35 U.S.C. §
103(a) as being unpatentable over Heinemann in view of Bettler ‘90, Sommer ‘92,
Puckett and Birnbaumer.
We reverse.
The rejection under 35 U.S.C. § 103(a):
According to the examiner (Answer30, page 6):
It would have been obvious to one of ordinary skill in the art at
the time the invention was made to isolate a human homolog of the rat
GluR5-231 sequence disclosed by Bettler [‘90] from a human cDNA
library, employing PCR amplification according to Puckett32, and
therewith to assay candidate agonists or antagonists of the human
receptor, according to Heinemann, because Bettler [‘90] teaches that
GluR5 has properties unique among the known glutamate receptors
(page 583, col. 2), because Puckett advocates the cloning of human
glutamate receptor genes in order to delimit their postulated
relationships to a variety of serious pathological conditions, and
29 We note the Answer contains a single new grounds of rejection over all appealed
claims. This new grounds of rejection was made to incorporate Sommer ‘92 (cited
by the examiner (Answer, page 4) as new prior art) into the statement of the
rejection.
30 Paper No. 23, mailed March 4, 1997,
31 The examiner states (Answer, page 5) that the GluR5-2 cDNA exhibits 86%
residue identify with appellants’ EAA3a SEQ ID NO:1 at the DNA level and the
predicted translation products are 98% identical. The examiner continues that the
identity between the rat clone of EAA3b is substantially equivalent to EAA3a except
that it differs at only a single nucleotide, resulting in a change at a single amino acid.
32 The examiner states (Answer, page 5) “Puckett discloses the cloning of a human
kainate-binding glutamate receptor, GluHI, which was obtained by PCR
amplification using primers derived from the published GluR1 sequence.” The
examiner states (Answer, page 14) that “Puckett evidences that PCR was a routine
and predictable procedure for the retrieval of homologous clones from mammalian
cDNA libraries.“ Puckett does not teach the isolation of GluR1 by use of PCR.
Puckett teaches the amplification of a probe [Puckett, page 7557, column 2 and
page 7558, Results, column 1] which is then used to screen a cDNA library under
reduced stringency hybridization [Puckett, bridging paragraphs, pages 7557-7558
and page 7558, Results, column 1].
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