Notice of Pre-AIA or AIA Status
The present application is being examined under the pre-AIA first to invent provisions.
Election/Restrictions
Applicant’s election without traverse of Group I, CD160 antigen precursor (SEQ ID NO: 21), immune cell, CD56+ natural killer cells, and “immune diseases or conditions” for (A) and (B) quantitative PCR analysis in the reply filed on 6/13/2025 is acknowledged.
Improper Markush
Claims 1-14 and 16-20 are rejected on the judicially-created basis that it contains an improper Markush grouping of alternatives. See In re Harnisch, 631 F.2d 716, 721-22 (CCPA 1980) and Ex parte Hozumi, 3 USPQ2d 1059, 1060 (Bd. Pat. App. & Int. 1984).
Claim 1 recites an improper Markush group wherein the nucleic acid sequence is selected from SEQ ID NO: 16-22, all claims depend from claim 1 and incorporate the recitation. The improper Markush grouping includes species of the claimed invention that do not share both a substantial structural feature and a common use that flows from the substantial structural feature. The members of the improper Markush grouping do not share a substantial feature and/or a common use that flows from the substantial structural feature for the following reasons: the members are different genes, each with a different nucleic acid sequence, expression pattern, encoding for a protein with different biological activity, and correlated with different cell types and states. The genes do not share a common structure or common activity, such that one would expect one gene to be capable of substituting for another to result in the identification of the same cell type and/or state. In response to this rejection, Applicant should either amend the claim(s) to recite only individual species or grouping of species that share a substantial structural feature as well as a common use that flows from the substantial structural feature, or present a sufficient showing that the species recited in the alternative of the claims(s) in fact share a substantial structural feature as well as a common use that flows from the substantial structural feature. This is a rejection on the merits and may be appealed to the Board of Patent Appeals and Interferences in accordance with 35 U.S.C. §134 and 37 CFR 41.31(a)(1) (emphasis provided).
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 1-14 and 16-20 are rejected under 35 U.S.C. 101 because the claimed invention is directed to a natural law without significantly more. The claim(s) recite(s) “a gene region specific for a cell type and/or a cell state from a human….wherein the amplicon comprises CA at one or more CpG positions of the gene region and the amplicon is specific for the cell type and/or cell state.” These claim limitations set forth the naturally occurring relationship between methylation in a gene region and a cell type or cell state. Claims 8, 9, 10, 11, 13, 14, 17, 18, 19, and 20 set forth additional and more specific relationships between specific genomic content or methylation and conditions or cell types or states. Claims 2, 3, 4, 5, 9, 10, 11, 13, 14, 18 and 19 set forth additional mental process judicial exceptions (comparing, diagnosis, compiling a knowledge base). These judicial exceptions are not integrated into a practical application because the elements in the claims in addition to the judicial exception do not use or apply the judicial exception in any way; the bisulfite treating and amplifying are mere data gathering steps. The claim(s) does/do not include additional elements that are sufficient to amount to significantly more than the judicial exceptions because the steps of bisulfite treating and amplifying with PCR are extra-solution data gathering steps recited at a high level of generality and that employ only well established, conventional techniques (Kristensen et al. overview of methods for detecting methylation (Clinical Chemistry 55:8, pages 1471–1483 (2009)).
This rejection could be overcome if the independent claims were amended to specifically require that the PCR employs a primer consisting of SEQ ID NO: 12 and/or SEQ ID NO: 13. The use of these primers to produce an amplicon was not well established before the filing date.
Claim Rejections - 35 USC § 112- Written Description
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-14 and 16-20 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claim 1 recites producing a gene amplicon from a gene region specific for a cell type and/or a cell state from a human by “amplifying…from a gene region comprising… SEQ ID NO: 21 (consonant with the election).” The claim sets forth that the amplicon is “from” a region comprising SEQ ID NO: 21, and as such encompasses amplicons from the genomic region that includes SEQ ID NO: 21 but does not require amplification of SEQ ID NO: 21. The claim also sets forth that the amplicon is “specific for the cell type and/or cell state.”
The disclosure only teaches a single amplicon “from” the region comprising SEQ ID NO: 21 that is specific for any cell state. Namely, the disclosure in Figure 5 teaches that the amplicon 1599 has a methylation pattern that is specific to CD56+ natural killer cells (NKC02 cells), where Amplicon 1599 is disclosed as instant SEQ ID NO: 21. In particular, chromatin is more accessible in amplicon 1599 (i.e. less methylated) than in other tested B cells, granulocytes, and monocytes.
Thus, the claims are drawn to producing a genus of amplicons from the “region” comprising SEQ ID NO: 21 that are specific for a cell type or a cell state where only a single amplicon specific for a single cell type is disclosed in the “region” comprising SEQ ID NO: 21.
To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of a complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, and any combination thereof. The specification states, that "the regions of CD160…are most accessible in CD56+ natural killer cells (NKC02)" (p. 23, lines 25-26).
Thus, the specification describes the elected species of accessible chromatin region as being able to function to identify CD56+ natural killer cells. No description is provided of other cell types or states that may be identified or quantified by analysis of a region of a CD160 gene. No description is provided of a region from CD160 gene that is diagnostic of a predisposition or disease. No description is provided of any regions that are diagnostic of a predisposition or diagnostic of a disease that is an autoimmune disease. The specification does not describe correlations for a representative number of regions to specific cell types, cell states, or diseases.
With regard to the elected invention of CD160, the example is representative of a specific region, SEQ ID NO: 21, that is correlated to a specific cell type, CD56+ NK cells, and not to any other specific cell states or diseases. The results are not predictive of all amplicons from the region containing SEQ ID NO: 21 for all cell types. There is no disclosure of diseases or disorders which can be diagnosed or predicted by measuring methylation within SEQ ID NO: 21 or any amplicon from the region comprising SEQ ID NO: 21. The specific relationship disclosed between SEQ ID NO: 21 and CD56+ NK cells cannot be extrapolated to other cell types, cell states or diseases. The specific relationships cannot be extrapolated to other regions and other cell types, cell states or diseases. Thus, it is impossible for one to extrapolate from the single example described herein those regions that would necessarily meet the structural/functional characteristics of the rejected claims.
The prior art does not appear to offset the deficiencies of the instant specification in that it does not describe a set of regions sufficient to describe the broadly claimed genus. The art of record discloses a few additional examples of accessible chromatin in regions of the genome, which are indicative of particular cell types. Baron et al (European Journal of Immunology, Vol. 37, No. 9, pages 2378-2389, 2007) disclose that multiple regions of COL6A3, GDF5, CAV1, ANXA6, FMOD, HIF1A, COL3A1 and BGN are indicative of the presence of keratinocytes, melanocytes, adipocytes, chondrocytes, fibroblasts, and mesenchymal stem cells when used in particular combinations (e.g., Fig. 2), but the reference is silent as to regions from the genomic locus comprising SEQ ID NO: 21 or CD106 and the identification of diseases or other subtypes of cells. A one-to-one correlation of a particular region and cell type is not present. Accordingly, examples in the art are not sufficient to support the description of the broadly claimed genus.
The specification does not clearly allow persons of ordinary skill in the art to recognize that applicant invented what is now is claimed. As discussed above, the skilled artisan cannot envision the detailed chemical structure of the encompassed genus of regions for detection, and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation or identification. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolating it.
Therefore, the skilled artisan would have reasonably concluded applicants were not in possession of the claimed invention for claims 1-14 and 16-20.
This amendment could be overcome by amending the claims to require that the method produces an amplicon that comprises a bisulfite treated SEQ ID NO: 21, and that the amplicon is specific for CD56+ natural killer cells.
Claim Rejections - 35 USC § 103
The following is a quotation of pre-AIA 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action:
(a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negated by the manner in which the invention was made.
This application currently names joint inventors. In considering patentability of the claims under pre-AIA 35 U.S.C. 103(a), the examiner presumes that the subject matter of the various claims was commonly owned at the time any inventions covered therein were made absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and invention dates of each claim that was not commonly owned at the time a later invention was made in order for the examiner to consider the applicability of pre-AIA 35 U.S.C. 103(c) and potential pre-AIA 35 U.S.C. 102(e), (f) or (g) prior art under pre-AIA 35 U.S.C. 103(a).
Claims 1, 6, 8, 12, 17 and 20 is/are rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Maiza et al. (J. Exp. Med. Vol. 178, September 1993, pages 1121-1126) in view of Olek et al. (WO 2006/094836), as evidenced by GenBank record AL390725, nucleotides 86911-87298; 25 July 2016.
Maiza et al. teaches that BY55 expression defines a unique subset mediating natural killer activity of circulating peripheral blood lymphocytes (Abstract; here note BY55 is a synonym for CD160), and that a subset of CD16+, CD56+ and CD57+ NK cells co-express BY55 (abstract and throughout). The reference teaches that BY55+ PBL were necessary for NK activity against standard target cells (p. 1124).
Maiza et al. do not teach producing an amplicon from a region comprising instant SEQ ID NO: 21 prior to bisulfite treatment. The claim is sufficiently broad so as to encompass producing an amplicon from the region, i.e. the claims do not require that the amplicon comprise bisulfite converted SEQ ID NO: 21, for example.
Olek teaches epigenetic characterization of cells and tissues that can be accomplished by bisulfite treating cells and then employing PCR to produce amplicons of gene regions. Olek teaches that cell type specific patterns have been identified in immune cell populations (p. 5-6). Olek et al. teach that for the cell types of interest, genes were chosen for analysis based on suspected relevance to particular cell types or cell states according to scientific literature. (p. 43). The reference teaches amplifying two portions of the target genes (two amplicons) from 200-500 base pairs long from bisulfite-treated DNA (p. 44).
Thus, it would have been prima facie obvious to have modified the methods taught by Maiza et al. so as to have included steps of obtaining genomic DNA from studied cells, bisulfite treating it, and amplifying amplicons in order to study methylation of DNA in the region of the genome encoding BY55. One would have been motivated to do so in order to study methylation in this marker that was known to be differentially expressed in a subset of cells, where the marker expression was necessary for natural killer activity. One would have been motivated to study to identify differential methylation patterns in amplicons from the region containing BY55, which is inherently the region comprising instant SEQ ID NO: 21.
Instant SEQ ID NO: 21 is inherently in the genomic region that contains DNA encoding BY55 (also known as CD160). This fact is supported at least by GenBank AL390725 which teaches a partion of SEQ ID NO: 1 that includes the CD160 gene, and where instant SEQ ID NO: 21 is fully complementary to nucleotides 86911-87298 of the disclosed sequence. See search result query attached to the end of this Office action.
Furthermore, the claim requires that the amplicon comprises CA at one or more CpG positions of the gene region, which would only occur in an instance when the original genomic DNA in at least one cell had at least one unmethylated CpG in the amplified region. As instant Figure 5 demonstrates that in NK cells, the amplicon from the CD160 region was largely unmethylated, the preponderance of evidence suggests that amplification from this region would result in an amplicon in which at least one CG was unmethylated, and therefore was bisulfite converted.
Claims 7 and 16 are rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Maiza et al. in view of Olek et al., as evidenced by GenBank AL390725 as applied to claims 1, 6, 8, 12, 17 and 20 above, and further in view of Van Engeland et al. (US 8969046).
The teachings of Maiza et al. in view of Olek et al. are given previously in this Office action and are fully incorporated here.
These do not teach a method wherein a region that is unspecific for the cell type and is from a region comprising a housekeeping gene and in particular GAPDH.
Van Engeland teaches that absolute copy number of a methylated marker may be determined relative to a reference gene such as GAPDH (Col. 25, lines 45-50).
It would have been obvious to have modified the method taught by Maiza in view of Olek so as to have also amplified GAPDH in order to provide a reference gene for determining the absolute copy number of the amplified portion from the region of the genome comprising the gene encoding BY55 (CD160).
Conclusion
No reference teaches that bisulfite treatment followed by amplicon with primers consisting of SEQ ID NO: 12 and 13 produces an amplicon that is specific to CD55+ natural killer cells.
Poli (2009, Immunology, 126, 458–465) taught that CD160 had strong expression in CD56dim NK cells and no expression in CD56bright NK cells.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Juliet Switzer whose telephone number is (571)272-0753. The examiner can normally be reached Monday to Thursday, 8:00 AM-3:30 PM.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Winston Shen can be reached at (571)-272-3157. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
Juliet Switzer
Primary Examiner
Art Unit 1682
/JULIET C SWITZER/Primary Examiner, Art Unit 1682
RESULT 1
AL390725/c
LOCUS AL390725 140348 bp DNA linear PRI 25-JUL-2016
DEFINITION Human DNA sequence from clone RP11-373C9 on chromosome 1 Contains
the 3' end of the ZNF364 gene for zinc finger protein 364, the
CD160 gene for CD160 antigen, the PDZK1 gene for PDZ domain
containing 1, the 3' end of the gene for putative G-protein coupled
receptor SH120 and a CpG island, complete sequence.
ACCESSION AL390725
VERSION AL390725.16
KEYWORDS HTG; CD160; CpG island; PDZK1; SH120; ZNF364.
SOURCE Homo sapiens (human)
ORGANISM Homo sapiens
Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi;
Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini;
Catarrhini; Hominidae; Homo.
REFERENCE 1 (bases 1 to 140348)
AUTHORS Wallis,J.
TITLE Direct Submission
JOURNAL Submitted (09-JAN-2009) Wellcome Trust Sanger Institute, Hinxton,
Cambridgeshire, CB10 1SA, UK. E-mail enquiries: vega\@sanger.ac.uk
Clone requests: Geneservice (http://www.geneservice.co.uk/) and
BACPAC Resources (http://bacpac.chori.org/)
COMMENT On Apr 11, 2003 this sequence version replaced AL390725.15.
-------------- Genome Center
Center: Wellcome Trust Sanger Institute
Center code: SC
Web site: http://www.sanger.ac.uk
Contact: vega\@sanger.ac.uk
--------------
This sequence was finished as follows unless otherwise noted: all
regions were either double-stranded or sequenced with an alternate
chemistry or covered by high quality data (i.e., phred quality >=
30); an attempt was made to resolve all sequencing problems, such
as compressions and repeats; all regions were covered by at least
one subclone; and the assembly was confirmed by restriction digest,
except on the rare occasion of the clone being a YAC.
The following abbreviations are used to associate primary accession
numbers given in the feature table with their source databases:
Em:, EMBL; Sw:, SWISSPROT; Tr:, TREMBL; Wp:, WORMPEP; Information
on the WORMPEP database can be found at
http://www.sanger.ac.uk/Projects/C_elegans/wormpep
This sequence was generated from part of bacterial clone contigs of
human chromosome 1, constructed by the Sanger Centre Chromosome 1
Mapping Group. Further information can be found at
http://www.sanger.ac.uk/HGP/Chr1
IMPORTANT: This sequence is not the entire insert of clone
RP11-373C9. It may be shorter because we sequence overlapping
sections only once, except for a short overlap.
During sequence assembly data is compared from overlapping clones.
Where differences are found these are annotated as variations
together with a note of the overlapping clone name. Note that the
variation annotation may not be found in the sequence submission
corresponding to the overlapping clone, as we submit sequences with
only a small overlap.
The true left end of clone RP11-373C9 is at 1 in this sequence. The
true right end of clone RP11-315I20 is at 16876 in this sequence.
The true right end of clone RP11-315I20 is at 16872 in this
sequence. The true right end of clone RP11-373C9 is at 140348 in
this sequence.
RP11-373C9 is from the library RPCI-11.2 constructed by the group
of Pieter de Jong. For further details see
http://bacpac.chori.org/
VECTOR: pBACe3.6.
FEATURES Location/Qualifiers
source 1..140348
/organism="Homo sapiens"
/mol_type="genomic DNA"
/db_xref="taxon:9606"
/chromosome="1"
/clone="RP11-373C9"
/clone_lib="RPCI-11.2"
gene order(AL160282.18:172461..172766,17946..18004,
22314..22371,34990..35198,53854..53925,55406..55478,
56416..56509,58807..58922,59920..62492)
/gene="RNF115"
/locus_tag="RP11-373C9.13-001"
mRNA join(AL160282.18:172461..172766,17946..18004,22314..22371,
34990..35198,53854..53925,55406..55478,56416..56509,
58807..58922,59920..62492)
/gene="RNF115"
/locus_tag="RP11-373C9.13-001"
/product="ring finger protein 115"
/note="match: ESTs: Em:AA748574.1 Em:AI341127.1
Em:AI660662.1 Em:AI825520.1 Em:AI968308.1 Em:AV752633.1
Em:AW439830.1 Em:AW966499.1 Em:BE877123.1 Em:BG025088.1
Em:BI224297.1 Em:BI670080.1 Em:BQ421607.1 Em:BQ582195.1
Em:BU155268.1 Em:BU197185.1 Em:BX381719.1 Em:CA310933.1
Em:CA447763.1;
match: cDNAs: Em:AF419857.1 Em:AF542552.1 Em:AK008329.1
Em:BC054049.2 Em:BC064903.1"
CDS join(AL160282.18:172665..172766,17946..18004,22314..22371,
34990..35198,53854..53925,55406..55478,56416..56509,
58807..58922,59920..60051)
/gene="RNF115"
/locus_tag="RP11-373C9.13-001"
/standard_name="OTTHUMP00000015602"
/note="match: proteins: Sw:Q9D0C1 Sw:Q9Y4L5 Tr:Q9Y4L5"
/codon_start=1
/product="ring finger protein 115"
/protein_id="CAI13717.1"
/db_xref="GDB:11508225"
/db_xref="GOA:Q9Y4L5"
/db_xref="HGNC:HGNC:18154"
/db_xref="InterPro:IPR001841"
/db_xref="InterPro:IPR013083"
/db_xref="InterPro:IPR018957"
/db_xref="UniProtKB/Swiss-Prot:Q9Y4L5"
/translation="MAEASAAGADSGAAVAAHRFFCHFCKGEVSPKLPEYICPRCESG
FIEEVTDDSSFLGGGGSRIDNTTTTHFAELWGHLDHTMFFQDFRPFLSSSPLDQDNRA
NERGHQTHTDFWGARPPRLPLGRRYRSRGSSRPDRSPAIEGILQHIFAGFFANSAIPG
SPHPFSWSGMLHSNPGDYAWGQTGLDAIVTQLLGQLENTGPPPADKEKITSLPTVTVT
QEQVDMGLECPVCKEDYTVEEEVRQLPCNHFFHSSCIVPWLELHDTCPVCRKSLNGED
STRQSQSTEASASNRFSNDSQLHDRWTF"
gene order(AL160282.18:172475..172766,17946..18004,
19847..19898,22314..22371,34990..35198,53854..53925,
55406..55478,56416..56509,58807..58922)
/gene="RNF115"
/locus_tag="RP11-373C9.13-002"
mRNA join(AL160282.18:172475..172766,17946..18004,19847..19898,
22314..22371,34990..35198,53854..53925,55406..55478,
56416..56509,58807..58922)
/gene="RNF115"
/locus_tag="RP11-373C9.13-002"
/product="ring finger protein 115"
/note="match: ESTs: Em:AA247930.1 Em:BE786633.1
Em:BX399452.1"
gene order(AL160282.18:172720..172766,17946..18004,
18110..18300,22314..22371,34990..35104)
/gene="RNF115"
/locus_tag="RP11-373C9.13-003"
mRNA join(AL160282.18:172720..172766,17946..18004,18110..18300,
22314..22371,34990..35104)
/gene="RNF115"
/locus_tag="RP11-373C9.13-003"
/product="ring finger protein 115"
/note="match: ESTs: Em:AV736218.1"
misc_feature 2001..140348
/note="annotated region of clone"
misc_feature 14872
/note="Clone_right_end: RP11-315I20"
misc_feature 14876
/note="Clone_right_end: RP11-315I20"
polyA_site 60558
/gene="RNF115"
/locus_tag="RP11-373C9.13-001"
regulatory 62456..62461
/regulatory_class="polyA_signal_sequence"
/gene="RNF115"
/locus_tag="RP11-373C9.13-001"
polyA_site 62485
/gene="RNF115"
/locus_tag="RP11-373C9.13-001"
polyA_site 62490
/gene="RNF115"
/locus_tag="RP11-373C9.13-001"
polyA_site 62492
/gene="RNF115"
/locus_tag="RP11-373C9.13-001"
misc_feature 65569..65577
/note="1329 bases of Tn10 transposon (J01829) removed
here. This sequence represents the duplicated flanking
sequence of the Tn10"
polyA_site complement(67763)
gene complement(order(67764..70921,78517..78658,87357..87445))
/gene="CD160"
/locus_tag="RP11-373C9.1-007"
mRNA complement(join(67764..70921,78517..78658,87357..87445))
/gene="CD160"
/locus_tag="RP11-373C9.1-007"
/product="CD160 molecule"
/note="match: cDNAs: Em:AK128370.1"
gene complement(order(67764..68431,70784..70921,75848..76174,
78517..78658,82010..82115,87357..87396))
/gene="CD160"
/locus_tag="RP11-373C9.1-006"
mRNA complement(join(67764..68431,70784..70921,75848..76174,
78517..78658,82010..82115,87357..87396))
/gene="CD160"
/locus_tag="RP11-373C9.1-006"
/product="CD160 molecule"
/note="match: ESTs: Em:BE464987.1 Em:BF433806.1
Em:BG743995.1 Em:BX283351.1;
match: cDNAs: Em:AF060981.1 Em:BC014465.1"
regulatory complement(67777..67782)
/regulatory_class="polyA_signal_sequence"
/gene="CD160"
/locus_tag="RP11-373C9.1-006"
CDS complement(join(68424..68431,70784..70921,75848..76174,
78517..78589))
/gene="CD160"
/locus_tag="RP11-373C9.1-006"
/standard_name="OTTHUMP00000015585"
/note="match: proteins: Sw:O95971"
/codon_start=1
Query Match 100.0%; Score 388; Length 140348;
Best Local Similarity 100.0%;
Matches 388; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 CTGCTCAGGTGAGGACAGGCTTCTCATGAGGTCCCTGAGAAACTTGCCTTTTGGAGGGAA 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 87298 CTGCTCAGGTGAGGACAGGCTTCTCATGAGGTCCCTGAGAAACTTGCCTTTTGGAGGGAA 87239
Qy 61 ATGTCCTCTGCCCTCTGGAGCCTGGGGAGAAGGTTATTTCTGCCCGCCAGACCAGCATGC 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 87238 ATGTCCTCTGCCCTCTGGAGCCTGGGGAGAAGGTTATTTCTGCCCGCCAGACCAGCATGC 87179
Qy 121 TCGCTTTTCTTCCATGGGCATTCAGGAATCCTGGCCCCATTCTGACATTCCTCAAATGGA 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 87178 TCGCTTTTCTTCCATGGGCATTCAGGAATCCTGGCCCCATTCTGACATTCCTCAAATGGA 87119
Qy 181 GGAATTCCTCAAATTACCAGAGGAAAGTTACCAAAGTTTAGATCTGCTGGAGCTCTTCAA 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 87118 GGAATTCCTCAAATTACCAGAGGAAAGTTACCAAAGTTTAGATCTGCTGGAGCTCTTCAA 87059
Qy 241 GGATTGGCCTGAGACAAGCCGGGAGGTGCCACGGGGCTTGGAGCTGGCCCTGTGAGGCAC 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 87058 GGATTGGCCTGAGACAAGCCGGGAGGTGCCACGGGGCTTGGAGCTGGCCCTGTGAGGCAC 86999
Qy 301 CTCCGGGGGAAGTTCATGTCCTAGGTGGTTCACGTCATGGACCTCTTGGAGGTCCGTGAA 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 86998 CTCCGGGGGAAGTTCATGTCCTAGGTGGTTCACGTCATGGACCTCTTGGAGGTCCGTGAA 86939
Qy 361 TAGATTTATTCATGGGATTTGTGAATTG 388
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Db 86938 TAGATTTATTCATGGGATTTGTGAATTG 86911