Abstract: A transgenic mouse comprising T30A, S32P, Q33L, N39D, and M470Q mutations in GPIIIa, as well as methods for making the transgenic mouse and methods for using the transgenic mouse to screen test compounds are described.

Abstract: A transgenic mouse comprising T30A, S32P, Q33L, N39D, and M470Q mutations in GPIIIa, as well as methods for making the transgenic mouse and methods for using the transgenic mouse to screen test compounds are described.

Abstract: A transgenic mouse comprising T30A, S32P, Q33L, N39D, and M470Q mutations in GPIIIa, as well as methods for making the transgenic mouse and methods for using the transgenic mouse to screen test compounds are described.

Abstract: According to this invention, a conventional pair of golf gloves is provided with pads across the palm portions thereof which abut the grip portion of a golf club shaft to automatically align the shaft for proper gripping. The guide pads are so positioned across the palm portions of the gloves that when the golf club head is soled on the ground and the upper and lower gripping hands of a golfer wearing the gloves receive the grip portion of the club shaft across the palms of the glove and against the pads, the shaft will lie diagonally across the roots of the fingers and when the hands are closed around the shaft with the guide pads cradling the grip portion of the golf club distal from the golf club head, an automatic proper gripping of the golf club will be insured. The guide pads are substantially parallel to the transverse creases of the hand, lying diagonally across the roots of the fingers. The pad on the first glove spans substantially the entire palm of the hand.

Abstract: Novel, substantially isolated isoforms of human platelet-endothelial cell adhesion molecule-1's, DNAs coding for transcripts that encode the novel isoforms and others, including a previously identified soluble isoform, methods of using such DNAs to make isoforms by expressing the DNA's, and promoter segments controlling transcription of human platelet-endothelial cell adhesion molecule-1 genes are provided. The novel isoforms differ from the complete human platelet-endothelial cell adhesion molecule-1's in lacking one or more segments near the C-terminus encoded by exons 10-15 of the genes for the full length molecules and arise in vivo from alternative splicing of the transcript from the genes.

Abstract: A glycoprotein, PECAM-1, and variants thereof can be obtained by expression in a transformed host cell of a polynucleotide coding for the glycoprotein or a variant polypeptide. PECAM-1 can also be isolated from cellular sources. An antibody specific for PECAM-1 or a PECAM variant can be produced via recombinant techniques, or can be obtained from a hybridoma.

Abstract: Isolated polynucleotide molecules and peptides encoded by these molecules can be used in the analysis of alloantigen phenotypes, as well as in diagnostic and therapeutic applications, relating to human platelet Pen polymorphism. By analyzing genomic DNA or amplified genomic DNA, or amplified cDNA derived from platelet mRNA, it is possible to type glycoprotein GPIIIa with regard to the Pen polymorphism, for example, in the context of diagnosing and treating clinical syndromes associated with GPIIIa-related immune responses.

Abstract: A glycoprotein, PECAM-1, and variants thereof can be obtained by expression in a transformed host cell of a polynucleotide coding for the glycoprotein or a variant polypeptide. PECAM-1 can also be isolated from cellular sources. An antibody specific for PECAM-1 or a PECAM variant can be produced via recombinant techniques, or can be obtained from a hybridoma.

Abstract: Isolated polynucleotide molecules and peptides encoded by these molecules can be used in the analysis of alloantigen phenotypes, as well as in diagnostic and therapeutic applications, relating to human platelet Pen polymorphism. By analyzing genomic DNA or amplified genomic DNA, or amplified cDNA derived from platelet mRNA, it is possible to type glycoprotein GPIIIa with regard to the Pen polymorphism, for example, in the context of diagnosing and treating clinical syndromes associated with GPIIIa-related immune responses.

Abstract: Isolated polynucleotide molecules, and peptides encoded by these molecules, can be used in the analysis of alloantigen phenotypes, as well as in diagnostic and therapeutic applications relating to human platelet Pl.sup.A polymorphism. In this vein, a method for typing blood cell and platelet membrane glycoproteins entails an analysis of amplified cDNA, encoded by platelet and red blood cell mRNA.

Abstract: Novel, substantially isolated isoforms of human platelet-endothelial cell adhesion molecule-1's, DNAs coding for transcripts that encode the novel isoforms and others, including a previously identified soluble isoform, methods of using such DNAs to make isoforms by expressing the DNA's, and promoter segments controlling transcription of human platelet-endothelial cell adhesion molecule-1 genes are provided. The novel isoforms differ from the complete human platelet-endothelial cell adhesion molecule-1's in lacking one or more segments near the C-terminus encoded by exons 10-15 of the genes for the full length molecules and arise in vivo from alternative splicing of the transcript from the genes.

Abstract: Isolated polynucleotide molecules and peptides encoded by these molecules can be used in the analysis of alloantigen phenotypes, as well as in diagnostic and therapeutic applications, relating to human platelet Bak polymorphism. By analyzing genomic DNA or amplified genomic DNA, or amplified cDNA derived from platelet mRNA, it is possible to type glycoprotein GPIIb with regard to the Bak polymorphism, for example, in the context of diagnosing and treating clinical syndromes associated with GPIIb-related immune responses.

Abstract: Based on the discovery of the amino acid and nucleotide differences which distinguish the Br.sup.a and Br.sup.b allelic forms of the membrane glycoprotein GPIa, and which comprise the diallelic Br platelet alloantigen system, compositions and methods are provided for determining the Br genotype and phenotype of individuals. Also provided, on the basis of this discovery, are compositions and methods for treating disorders associated with Br alloantigen incompatibility, such as the bleeding disorders post-transfusion purpura, post-transfusion platelet refractoriness, and neonatal alloimmune thrombocytopenic purpura. The two allelic forms of GPIa differ by a single amino acid. The Br.sup.a allelic form has Lys at position 505 in the sequence of the mature GPIa. The Br.sup.b allelic form has Glu at the same position. This amino acid difference is due to a single change, from A for the Br.sup.a allele to G for the Br.sup.b allele, in the GPIa gene.

Abstract: Isolated polynucleotide molecules and peptides encoded by these molecules can be used in the analysis of alloantigen phenotypes, as well as in diagnostic and therapeutic applications, relating to human platelet Bak polymorphism. By analyzing genomic DNA or amplified genomic DNA, or amplified cDNA derived from platelet mRNA, it is possible to type glycoprotein GPIIb with regard to the Bak polymorphism, for example, in the context of diagnosing and treating clinical syndromes associated with GPIIb-related immune responses.

Abstract: Antibodies which distinguish between the Pl.sup.A1 form of GPIIIa and the Pl.sup.A2 form of GPIIIa can be used in the analysis of alloantigen phenotypes, as well as in diagnostic applications relating to human platelet Pl.sup.A polymorphism.

Abstract: Isolated polynucleotide molecules, and peptides encoded by those molecules, can be used in the analysis of alloantigen phenotypes, as well as in diagnostic and therapeutic applications relating to human platelet Pl.sup.A polymorphism. In this vein, a method for typing blood cell and platelet membrane glycoproteins entails an analysis of amplified cDNA, encoded by platelet and red blood cell mRNA.