Government-Owned Inventions; Availability for Licensing, 45229-45231 [E8-17812]

Download as PDF Federal Register / Vol. 73, No. 150 / Monday, August 4, 2008 / Notices Frequency of response: Applicants may submit applications for published receipt dates. If awarded, annual progress is reported and trainees may be appointed or reappointed. Affected Public: Individuals or Households; Business or other for-profit; Not-forprofit institutions; Federal Government; and State, Local or Tribal Government. Type of Respondents: Adult scientific trainees and professionals. The annual reporting burden is as follows: Estimated Number of Respondents: 34,454; Estimated Number of Responses per Respondent: 1; Average Burden Hours per Response: 4.1; and Estimated Total Annual Burden Hours Requested: 142,301. The annualized cost to respondents is estimated at: $4,980,535. Request for Comments: Written comments and/or suggestions from the public and affected agencies are invited on one or more of the following points: (1) Whether the proposed collection of information is necessary for the proper performance of the function of the agency, including whether the information will have practical utility; (2) The accuracy of the agency’s estimate of the burden of the proposed collection of information, including the validity of the methodology and assumptions used; (3) Ways to enhance the quality, utility, and clarity of the information to be collected; and (4) Ways to minimize the burden of the collection of information on those who are to respond, including the use of appropriate automated, electronic, mechanical, or other technological collection techniques or other forms of information technology. Direct Comments to OMB: Written comments and/or suggestions regarding the item(s) contained in this notice, especially regarding the estimated public burden and associated response time should be sent via e-mail to OIRA_submission@omb.eop.gov or by fax to 202–395–6974, Attention: Desk Officer for NIH. To request more information on the proposed project or to obtain a copy of the data collection plans and instruments, contact Ms. Mikia Currie, Project Clearance Branch, Office of Policy for Extramural Research Administration, NIH, Rockledge 1 Building, Suite 350, 6705 Rockledge Drive, Bethesda, MD 20892–7974, or call non-toll-free number (301) 435– 0941, or e-mail your request, including your address to: curriem@od.nih.gov. Comments Due Date: Comments regarding this information collection are best assured of having their full effect if received within 30 days of the date of this publication. Dated: July 24, 2008. Pam Gilden, Division of Grants Policy, Office of Policy for Extramural Research Administration, Office of Extramural Research, National Institutes of Health. [FR Doc. E8–17727 Filed 8–1–08; 8:45 am] BILLING CODE 4140–01–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health Government-Owned Inventions; Availability for Licensing National Institutes of Health, Public Health Service, HHS. ACTION: Notice. AGENCY: SUMMARY: The inventions listed below are owned by an agency of the U.S. Government and are available for licensing in the U.S. in accordance with 35 U.S.C. 207 to achieve expeditious commercialization of results of federally-funded research and development. Foreign patent applications are filed on selected inventions to extend market coverage for companies and may also be available for licensing. ADDRESSES: Licensing information and copies of the U.S. patent applications listed below may be obtained by writing to the indicated licensing contact at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852–3804; telephone: 301/ 496–7057; fax: 301/402–0220. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications. SUPPLEMENTARY INFORMATION: 45229 Antibodies and Antisera Recognizing Members of the ArfGap Family of Proteins Description of Technology The technology involves antibodies and antisera that recognize members of the ArfGap protein family, including the following proteins: • ACAP1, which is related to ASAP1, a putative oncogene that regulates cancer cell invasion into normal tissues. ACAP1 regulates integrins, which are critical for cell movement associated with cancer cell invasion and is a target of the oncogene Akt. • ACAP2, which is related to ASAP1, a putative oncogene that regulates cancer cell invasion into normal tissues. • AGAP2 (also known as PIKE–A), ASAP1 (also called AMAP1 and DDEFl), and ASAP3 all exhibit elevated expression levels in cancer cells compared to non-transformed cells and as putative oncogenes have been implicated as regulators of cancer cell invasion into normal tissues and contributors to brain, eye and breast, and liver cancers, respectively. • ARAP1 (also called Centaurin Delta 2), which has been implicated as a regulator of epidermal growth factor receptor, which plays important roles in several malignancies. • ARAP2 (also called Centaurin Delta 1), GIT1 and GIT2; all three of which have been implicated as regulators of cell migration required for cancer cell invasion into normal tissues and metastasis. • ARAP3, a target of the Src oncogene, has been implicated as a regulator of cell movement and signaling. • ArfGAP1, which is critical to cell function, including protein trafficking. • ASAP2 (also known as PAG3 or as Pap in the 1999 Molecular and Cellular Biology publication), is highly related to ASAP1, which has been implicated as a regulator of cancer cell invasion into normal tissues. The table below summarizes the antibodies and antisera available against different ArfGap proteins. Each material has been raised or generated to the peptide sequence listed. ANTIBODIES AND ANTISERA RECOGNIZING ARFGAP PROTEINS pwalker on PROD1PC71 with NOTICES ArfGap member Antibody/serum ID (Alt. Name) Antibody source Peptide sequence (ID) ACAP1 .......... ACAP2 .......... AGAP2 .......... 1241 (Arf6-specific GAP) ....... 1288 ........................................ 4569, 4571 ............................. Rabbit ........... Rabbit ........... Rabbit ........... ARAP1 .......... 1153 ........................................ Rabbit ........... RPRGQPPVPPKPSIR(556) .................................................... REKGDESEKLDKKSS(365) .................................................... ERVDDPELQDSI and PLSREPPPSPMVKKQ ....................... (483) ..................................................................................... SLIPLRGSENEMRRSV ........................................................... VerDate Aug<31>2005 16:50 Aug 01, 2008 Jkt 214001 PO 00000 Frm 00025 Fmt 4703 Sfmt 4703 E:\FR\FM\04AUN1.SGM 04AUN1 HHS Ref. No. E–244–2008/0 E–242–2008/0 E–222–2008/0 E–220–2008/0 45230 Federal Register / Vol. 73, No. 150 / Monday, August 4, 2008 / Notices ANTIBODIES AND ANTISERA RECOGNIZING ARFGAP PROTEINS—Continued ArfGap member Antibody/serum ID (Alt. Name) Antibody source Peptide sequence (ID) ARAP2 .......... 1185, 1187 ............................. Rabbit ........... E–220–2008/1 ARAP3 .......... Rabbit ........... ArfGAP1 ....... 862, 863, 864, 865 (CENTD3/ DRAG1). 870 .......................................... RSRTLPKELQDEQILK ............................................................ (1689) and ANVHKTKKNDDPSKDY ................................... DKDPPFPKGVIPLTAIE and EPVYEEPVYEEVGAFPE ......... E–243–2008/0 ASAP1 .......... 642, 645, 551, 553 ................. Rabbit ........... ASAP1a ........ 574 .......................................... Rabbit ........... ASAP1 .......... ................................................. Mouse .......... ASAP2 .......... 1267, 4574, 4575, 578 ........... Rabbit ........... ASAP3 .......... Anti-ASAP3 (DDEFL1/UPLC1/ ACAP4). ................................................. ................................................. Rabbit ........... EWSLESSPAQNWTPPQP ..................................................... (123) ..................................................................................... VELAPKPQVGELPPKPG (962), DQDRTALQKVKKSVAC, and murine protein residues 325–725; 440–724. LSKKPPPPPPGHKRTL .......................................................... (837) ..................................................................................... VELAPKPQVGELPPKPG ....................................................... (962) ..................................................................................... DEKLQPSPNRREDRP(706) and human protein fragment of the PH, Arf GAP and Ankyrin repeat domains. WVISTEPGSDSEEDEEKR ..................................................... Rabbit ........... Rabbit ........... LRQPPGPVPTPPLPSER and RKTVPPEPGAPVDF ............. RSSEVCADCSGPDPS and KVNNNLSDELRIMQKK ............. GIT1 .............. GIT2 .............. Applications • Immunoblotting and other procedures to identify the ArfGap proteins in cells and tissues; • Identifying tumors, such as those found in brain, breast, eye and liver cancers, based on protein expression levels; • Examining the invasive behavior of tumor cells. Development Status The antibodies and antisera have been raised or generated to the particular peptide sequence given in the table above. These are available as Research Tools. Inventors Paul A. Randazzo et al. (NCI). pwalker on PROD1PC71 with NOTICES Relevant Publications These antibodies and antisera are further described in the following research articles: 1. Andreev J, Simon JP, Sabatini DD, Kam J, Plowman G, Randazzo PA, Schlessinger J. Identification of a new Pyk2 target protein with Arf-GAP activity. Mol Cell Biol. 1999 Mar;19(3):2338–2350. 2. Bharti S, Inoue H, Bharti K, Hirsch DS, Nie Z, Yoon HY, Artym V, Yamada KM, Mueller SC, Barr VA, Randazzo PA. Src-dependent phosphorylation of ASAP1 regulates podosomes. Mol Cell Biol. 2007 Dec;27(23):8271–8283. 3. Dai J, Li J, Bos E, Porcionatto M, Premont RT, Bourgoin S, Peters PJ, Hsu VW. ACAP1 promotes endocytic recycling by recognizing recycling sorting signals. Dev Cell. 2004 Nov;7(5):771–776. VerDate Aug<31>2005 16:50 Aug 01, 2008 Jkt 214001 Rabbit ........... 4. Ha VL et al. ASAP3 is a focal adhesion-associated Arf GAP that functions in cell migration and invasion. J Biol Chem. 2008 May 30;283(22):14915–14926. 5. I ST, Nie Z, Stewart A, Najdovska M, Hall NE, He H, Randazzo PA, Lock P. ARAP3 is transiently tyrosine phosphorylated in cells attaching to fibronectin and inhibits cell spreading in a RhoGAP-dependent manner. J Cell Sci. 2004 Dec 1;117(Pt 25):6071– 6084. 6. Inoue H and Randazzo PA. Arf GAPs and their interacting proteins. Traffic 2007 Nov;8(11):1465–1475. 7. Li J, Ballif BA, Powelka AM, Dai J, Gygi SP, Hsu VW. Phosphorylation of ACAP1 by Akt regulates the stimulation-dependent recycling of integrin beta1 to control cell migration. Dev Cell. 2005 Nov;9(5):663–673. 8. Miura K, Jacques KM, Stauffer S, Kubosaki A, Zhu K, Hirsch DS, Resau J, Zheng Y, Randazzo PA. ARAP1: a point of convergence for Arf and Rho signaling. Mol Cell 2002 Jan;9(1):109– 119. 9. Nie Z, Fei J, Premont RT, Randazzo PA. The Arf GAPs AGAP1 and AGAP2 distinguish between the adaptor protein complexes AP–1 and AP–3. J Cell Sci. 2005 Aug 1;118(Pt 15):3555–3566. 10. Randazzo PA, Andrade J, Miura K, Brown MT, Long YQ, Stauffer S, Roller P, Cooper JA. The Arf GTPaseactivating protein ASAP1 regulates the actin cytoskeleton. Proc Natl Acad Sci USA. 2000 Apr 11;97(8):4011– 4016. 11. Liu W, Duden R, Phair RD, Lippincott-Schwartz J. ArfGAP1 dynamics and its role in COPI coat assembly on Golgi membranes of PO 00000 Frm 00026 Fmt 4703 Sfmt 4703 HHS Ref. No. E–220–2008/2 E–221–2008/0 E–221–2008/0 E–252–2008/0 E–221–2008/1 E–221–2008/2 E–245–2008/0 E–245–2008/1 living cells. J. Cell Biol. 2005 Mar 28;168(7):1053–1063. 12. Yoon MY, Miura K, Cuthbert EJ, Davis KK, Ahvazi B, Casanova JE, Randazzo PA. ARAP2 effects on the actin cytoskeleton are dependent on Arf6-specific GTPase-activatingprotein activity and binding to RhoA– GTP. J Cell Sci. 2006 Nov 15;119(Pt 22):4650–4666. Patent Status Patent protection is not being pursued for this technology. • HHS Reference No. E–220–2008/ 0—Research Tool. • HHS Reference No. E–220–2008/ 1—Research Tool. • HHS Reference No. E–220–2008/ 2—Research Tool. • HHS Reference No. E–221–2008/ 0—Research Tool. • HHS Reference No. E–221–2008/ 1—Research Tool. • HHS Reference No. E–221–2008/ 2—Research Tool. • HHS Reference No. E–222–2008/ 0—Research Tool. • HHS Reference No. E–242–2008/ 0—Research Tool. • HHS Reference No. E–243–2008/ 0—Research Tool. • HHS Reference No. E–244–2008/ 0—Research Tool. • HHS Reference No. E–245–2008/ 0—Research Tool. • HHS Reference No. E–245–2008/ 1—Research Tool. • HHS Reference No. E–252–2008/ 0—Research Tool. Licensing Status Available for non-exclusive biological materials licensing only. E:\FR\FM\04AUN1.SGM 04AUN1 Federal Register / Vol. 73, No. 150 / Monday, August 4, 2008 / Notices Licensing Contact Surekha Vathyam, Ph.D.; 301–435– 4076; vathyams@mail.nih.gov. Dated: July 28, 2008. Richard U. Rodriguez, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. E8–17812 Filed 8–1–08; 8:45 am] BILLING CODE 4140–01–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health Prospective Grant of Exclusive License: The Development of Human Therapeutics for the Treatment of Depression National Institutes of Health, Public Health Service, HHS. ACTION: Notice. AGENCY: SUMMARY: This notice, in accordance with 35 U.S.C. 209(c)(1) and 37 CFR Part 404.7(a)(1)(i), that the National Institutes of Health, Department of Health and Human Services, is contemplating the grant of an exclusive patent license to practice the inventions embodied in U.S. Patent Application 11/137,114 entitled ‘‘Scopolamine For The Treatment Of Depression And Anxiety’’ [HHS Ref. E–175–2004/0–US– 01], PCT Application PCT/US2006/ 019335 [HHS Ref. E–175–2004/0–PCT– 02] and all continuing applications and foreign counterparts (Europe, Australia and Canada), to Transcept Pharmaceuticals, Inc., which has offices in Pt. Richmond, CA. The patent rights in these inventions have been assigned to and/or exclusively licensed to the Government of the United States of America. The prospective exclusive license territory may be worldwide, and the field of use may be limited to: A worldwide exclusive license for the use of scopolamine for treatment of depression, including major depressive disorders (MDD), wherein the administration of scopolamine is intravenous, through the buccal membrane, intranasal, intramuscular or through a skin patch. Only written comments and/or applications for a license which are received by the NIH Office of Technology Transfer on or before October 3, 2008, will be considered. ADDRESSES: Requests for copies of the patent application, inquiries, comments, and other materials relating to the contemplated exclusive license should be directed to: David A. Lambertson, Ph.D., Technology Licensing Specialist, pwalker on PROD1PC71 with NOTICES DATES: VerDate Aug<31>2005 16:50 Aug 01, 2008 Jkt 214001 45231 Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, MD 20852–3804; Telephone: (301) 435– 4632; Facsimile: (301) 402–0220; E-mail: lambertsond@od.nih.gov. DEPARTMENT OF HOMELAND SECURITY The invention concerns the use of scopolamine for the treatment of depression, including major depressive disorders (MDD). Although scopolamine has been employed in the treatment of nausea and motion sickness, the suitability of scopolamine for treating MDD was unrecognized prior to this invention. Current MDD treatments can be ineffective in large percentage of patients and typically do not take effect until 4 weeks after administration. In contrast, treatment with scopolamine has a wide-ranging and rapid effect, suggesting it can be effective either as a stand alone treatment or as a treatment for patients who are unresponsive to currently available drugs. A Cooperative Research and Development Agreement (CRADA) is simultaneously being negotiated to accompany the exclusive license agreement. The CRADA will involve the further development of the licensed technology between the National Institute of Mental Health and Transcept. The prospective exclusive license will be royalty bearing and will comply with the terms and conditions of 35 U.S.C. 209 and 37 CFR part 404.7. The prospective exclusive license may be granted unless within sixty (60) days from the date of this published notice, the NIH receives written evidence and argument that establishes that the grant of the license would not be consistent with the requirements of 35 U.S.C. 209 and 37 CFR part 404.7. Applications for a license in the field of use filed in response to this notice will be treated as objections to the grant of the contemplated exclusive license. Applicants may also contact the National Institute of Mental Health regarding the CRADA opportunity. Comments and objections submitted to this notice will not be made available for public inspection and, to the extent permitted by law, will not be released under the Freedom of Information Act, 5 U.S.C. 552. National Preparedness for Response Exercise Program SUPPLEMENTARY INFORMATION: Dated: July 29, 2008. Richard U. Rodriguez, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. E8–17817 Filed 8–1–08; 8:45 am] BILLING CODE 4140–01–P PO 00000 Frm 00027 Fmt 4703 Sfmt 4703 Coast Guard [Docket No. USCG–2008–0521] Coast Guard, DHS. Notice; request for public comment. AGENCY: ACTION: SUMMARY: The Coast Guard, the Pipeline and Hazardous Materials Safety Administration, the Environmental Protection Agency, and the Minerals Management Service, in concert with representatives from various State governments, industry, environmental interest groups, and the general public, developed the National Preparedness for Response Exercise Program (PREP) Guidelines to reflect the consensus agreement of the entire oil spill response community. This notice announces the PREP 5-year exercise cycle, 2009 through 2013, and requests comments from the public, and requests volunteers from industry to participate in the scheduled PREP Area exercises. The new schedule adjustment from 3 years to 5 years was created to align with the Department of Homeland Security’s National Exercise 5-year Schedule. Comments and related material must reach the Docket Management Facility on or before October 3, 2008. ADDRESSES: You may submit comments identified by Coast Guard docket number USCG–2008–0521 to the Docket Management Facility at the U.S. Department of Transportation. To avoid duplication, please use only one of the following methods: (1) Online: https:// www.regulations.gov. (2) Mail: Docket Management Facility (M–30), U.S. Department of Transportation, West Building Ground Floor, Room W12–140, 1200 New Jersey Avenue, SE., Washington, DC 20590– 0001. (3) Hand delivery: Same as mail address above, between 9 a.m. and 5 p.m., Monday through Friday, except Federal holidays. The telephone number is 202–366–9329. (4) Fax: 202–493–2251. FOR FURTHER INFORMATION CONTACT: If you have questions on this notice, or need general information regarding the PREP or the 5-year exercise schedule, contact Lieutenant Shawn Essert, Office of Contingency Exercises (CG–535), U.S. Coast Guard, telephone 202–372–2149, or e-mail shawn.g.essert@uscg.mil. If DATES: E:\FR\FM\04AUN1.SGM 04AUN1

Agencies

[Federal Register Volume 73, Number 150 (Monday, August 4, 2008)]
[Notices]
[Pages 45229-45231]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E8-17812]


-----------------------------------------------------------------------

DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health


Government-Owned Inventions; Availability for Licensing

AGENCY: National Institutes of Health, Public Health Service, HHS.

ACTION: Notice.

-----------------------------------------------------------------------

SUMMARY: The inventions listed below are owned by an agency of the U.S. 
Government and are available for licensing in the U.S. in accordance 
with 35 U.S.C. 207 to achieve expeditious commercialization of results 
of federally-funded research and development. Foreign patent 
applications are filed on selected inventions to extend market coverage 
for companies and may also be available for licensing.

ADDRESSES: Licensing information and copies of the U.S. patent 
applications listed below may be obtained by writing to the indicated 
licensing contact at the Office of Technology Transfer, National 
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, 
Maryland 20852-3804; telephone: 301/496-7057; fax: 301/402-0220. A 
signed Confidential Disclosure Agreement will be required to receive 
copies of the patent applications.

SUPPLEMENTARY INFORMATION: 

Antibodies and Antisera Recognizing Members of the ArfGap Family of 
Proteins

Description of Technology

    The technology involves antibodies and antisera that recognize 
members of the ArfGap protein family, including the following proteins:
     ACAP1, which is related to ASAP1, a putative oncogene that 
regulates cancer cell invasion into normal tissues. ACAP1 regulates 
integrins, which are critical for cell movement associated with cancer 
cell invasion and is a target of the oncogene Akt.
     ACAP2, which is related to ASAP1, a putative oncogene that 
regulates cancer cell invasion into normal tissues.
     AGAP2 (also known as PIKE-A), ASAP1 (also called AMAP1 and 
DDEFl), and ASAP3 all exhibit elevated expression levels in cancer 
cells compared to non-transformed cells and as putative oncogenes have 
been implicated as regulators of cancer cell invasion into normal 
tissues and contributors to brain, eye and breast, and liver cancers, 
respectively.
     ARAP1 (also called Centaurin Delta 2), which has been 
implicated as a regulator of epidermal growth factor receptor, which 
plays important roles in several malignancies.
     ARAP2 (also called Centaurin Delta 1), GIT1 and GIT2; all 
three of which have been implicated as regulators of cell migration 
required for cancer cell invasion into normal tissues and metastasis.
     ARAP3, a target of the Src oncogene, has been implicated 
as a regulator of cell movement and signaling.
     ArfGAP1, which is critical to cell function, including 
protein trafficking.
     ASAP2 (also known as PAG3 or as Pap in the 1999 Molecular 
and Cellular Biology publication), is highly related to ASAP1, which 
has been implicated as a regulator of cancer cell invasion into normal 
tissues.
    The table below summarizes the antibodies and antisera available 
against different ArfGap proteins. Each material has been raised or 
generated to the peptide sequence listed.

                               Antibodies and Antisera Recognizing ArfGap Proteins
----------------------------------------------------------------------------------------------------------------
                          Antibody/serum ID
     ArfGap member           (Alt. Name)          Antibody source       Peptide sequence (ID)      HHS Ref. No.
----------------------------------------------------------------------------------------------------------------
ACAP1.................  1241 (Arf6-specific    Rabbit...............  RPRGQPPVPPKPSIR(556).....     E-244-2008/0
                         GAP).
ACAP2.................  1288.................  Rabbit...............  REKGDESEKLDKKSS(365).....     E-242-2008/0
AGAP2.................  4569, 4571...........  Rabbit...............  ERVDDPELQDSI and              E-222-2008/0
                                                                       PLSREPPPSPMVKKQ.
                                                                       (483)...................
ARAP1.................  1153.................  Rabbit...............  SLIPLRGSENEMRRSV.........     E-220-2008/0

[[Page 45230]]

 
ARAP2.................  1185, 1187...........  Rabbit...............  RSRTLPKELQDEQILK.........     E-220-2008/1
                                                                       (1689) and
                                                                       ANVHKTKKNDDPSKDY.
ARAP3.................  862, 863, 864, 865     Rabbit...............  DKDPPFPKGVIPLTAIE and         E-220-2008/2
                         (CENTD3/DRAG1).                               EPVYEEPVYEEVGAFPE.
ArfGAP1...............  870..................  Rabbit...............  EWSLESSPAQNWTPPQP........     E-243-2008/0
                                                                       (123)...................
ASAP1.................  642, 645, 551, 553...  Rabbit...............  VELAPKPQVGELPPKPG (962),      E-221-2008/0
                                                                       DQDRTALQKVKKSVAC, and
                                                                       murine protein residues
                                                                       325-725; 440-724.
ASAP1a................  574..................  Rabbit...............  LSKKPPPPPPGHKRTL.........     E-221-2008/0
                                                                       (837)...................
ASAP1.................  .....................  Mouse................  VELAPKPQVGELPPKPG........     E-252-2008/0
                                                                       (962)...................
ASAP2.................  1267, 4574, 4575, 578  Rabbit...............  DEKLQPSPNRREDRP(706) and      E-221-2008/1
                                                                       human protein fragment
                                                                       of the PH, Arf GAP and
                                                                       Ankyrin repeat domains.
ASAP3.................  Anti-ASAP3 (DDEFL1/    Rabbit...............  WVISTEPGSDSEEDEEKR.......     E-221-2008/2
                         UPLC1/ACAP4).
GIT1..................  .....................  Rabbit...............  LRQPPGPVPTPPLPSER and         E-245-2008/0
                                                                       RKTVPPEPGAPVDF.
GIT2..................  .....................  Rabbit...............  RSSEVCADCSGPDPS and           E-245-2008/1
                                                                       KVNNNLSDELRIMQKK.
----------------------------------------------------------------------------------------------------------------

Applications

     Immunoblotting and other procedures to identify the ArfGap 
proteins in cells and tissues;
     Identifying tumors, such as those found in brain, breast, 
eye and liver cancers, based on protein expression levels;
     Examining the invasive behavior of tumor cells.

Development Status

    The antibodies and antisera have been raised or generated to the 
particular peptide sequence given in the table above. These are 
available as Research Tools.

Inventors

    Paul A. Randazzo et al. (NCI).

Relevant Publications

    These antibodies and antisera are further described in the 
following research articles:

1. Andreev J, Simon JP, Sabatini DD, Kam J, Plowman G, Randazzo PA, 
Schlessinger J. Identification of a new Pyk2 target protein with Arf-
GAP activity. Mol Cell Biol. 1999 Mar;19(3):2338-2350.
2. Bharti S, Inoue H, Bharti K, Hirsch DS, Nie Z, Yoon HY, Artym V, 
Yamada KM, Mueller SC, Barr VA, Randazzo PA. Src-dependent 
phosphorylation of ASAP1 regulates podosomes. Mol Cell Biol. 2007 
Dec;27(23):8271-8283.
3. Dai J, Li J, Bos E, Porcionatto M, Premont RT, Bourgoin S, Peters 
PJ, Hsu VW. ACAP1 promotes endocytic recycling by recognizing recycling 
sorting signals. Dev Cell. 2004 Nov;7(5):771-776.
4. Ha VL et al. ASAP3 is a focal adhesion-associated Arf GAP that 
functions in cell migration and invasion. J Biol Chem. 2008 May 
30;283(22):14915-14926.
5. I ST, Nie Z, Stewart A, Najdovska M, Hall NE, He H, Randazzo PA, 
Lock P. ARAP3 is transiently tyrosine phosphorylated in cells attaching 
to fibronectin and inhibits cell spreading in a RhoGAP-dependent 
manner. J Cell Sci. 2004 Dec 1;117(Pt 25):6071-6084.
6. Inoue H and Randazzo PA. Arf GAPs and their interacting proteins. 
Traffic 2007 Nov;8(11):1465-1475.
7. Li J, Ballif BA, Powelka AM, Dai J, Gygi SP, Hsu VW. Phosphorylation 
of ACAP1 by Akt regulates the stimulation-dependent recycling of 
integrin beta1 to control cell migration. Dev Cell. 2005 Nov;9(5):663-
673.
8. Miura K, Jacques KM, Stauffer S, Kubosaki A, Zhu K, Hirsch DS, Resau 
J, Zheng Y, Randazzo PA. ARAP1: a point of convergence for Arf and Rho 
signaling. Mol Cell 2002 Jan;9(1):109-119.
9. Nie Z, Fei J, Premont RT, Randazzo PA. The Arf GAPs AGAP1 and AGAP2 
distinguish between the adaptor protein complexes AP-1 and AP-3. J Cell 
Sci. 2005 Aug 1;118(Pt 15):3555-3566.
10. Randazzo PA, Andrade J, Miura K, Brown MT, Long YQ, Stauffer S, 
Roller P, Cooper JA. The Arf GTPase-activating protein ASAP1 regulates 
the actin cytoskeleton. Proc Natl Acad Sci USA. 2000 Apr 11;97(8):4011-
4016.
11. Liu W, Duden R, Phair RD, Lippincott-Schwartz J. ArfGAP1 dynamics 
and its role in COPI coat assembly on Golgi membranes of living cells. 
J. Cell Biol. 2005 Mar 28;168(7):1053-1063.
12. Yoon MY, Miura K, Cuthbert EJ, Davis KK, Ahvazi B, Casanova JE, 
Randazzo PA. ARAP2 effects on the actin cytoskeleton are dependent on 
Arf6-specific GTPase-activating-protein activity and binding to RhoA-
GTP. J Cell Sci. 2006 Nov 15;119(Pt 22):4650-4666.

Patent Status

    Patent protection is not being pursued for this technology.
     HHS Reference No. E-220-2008/0--Research Tool.
     HHS Reference No. E-220-2008/1--Research Tool.
     HHS Reference No. E-220-2008/2--Research Tool.
     HHS Reference No. E-221-2008/0--Research Tool.
     HHS Reference No. E-221-2008/1--Research Tool.
     HHS Reference No. E-221-2008/2--Research Tool.
     HHS Reference No. E-222-2008/0--Research Tool.
     HHS Reference No. E-242-2008/0--Research Tool.
     HHS Reference No. E-243-2008/0--Research Tool.
     HHS Reference No. E-244-2008/0--Research Tool.
     HHS Reference No. E-245-2008/0--Research Tool.
     HHS Reference No. E-245-2008/1--Research Tool.
     HHS Reference No. E-252-2008/0--Research Tool.

Licensing Status

    Available for non-exclusive biological materials licensing only.

[[Page 45231]]

Licensing Contact

    Surekha Vathyam, Ph.D.; 301-435-4076; vathyams@mail.nih.gov.

    Dated: July 28, 2008.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. E8-17812 Filed 8-1-08; 8:45 am]
BILLING CODE 4140-01-P
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