Abstract: Novel direct thrombin inhibitors are provided herein, along with methods for their use as anticoagulants. The direct thrombin inhibitors described herein are useful in treating and/or preventing thromboembolism and bleeding or clotting disorders. Also provided herein are methods for inhibiting thrombin in a cell using the compounds and compositions described herein.

Abstract: The invention relates to compositions and methods for effecting male contraception.

Abstract: The invention relates to compositions and methods for effecting male contraception.

Abstract: The invention relates to compositions and methods for effecting male contraception.

Abstract: The invention relates to compositions and methods for effecting male contraception.

Abstract: The present invention relates to compositions and methods for modulating conception in animals. More particularly, the composition modulates mRNA degradation during gametogenesis and early development. Yet further, the present invention relates to pharmaceutical compositions and methods for modulating diseases of the reproductive organs, such as hyperproliferative diseases.

Abstract: Isolated GDF-9 regulatory sequences are disclosed, as well as methods of using the sequences to modulate tissue-specific expression of genes. The GDF-9 regulatory sequences include, for example, enhancer and promoter elements that naturally drive transcription of GDF-9 in specific tissues. The GDF-9 regulatory sequences can be derived from the untranscribed upstream (e.g., first 10 kilobases) and downstream regions, and transcribed, untranslated regions of a GDF-9 gene.

Abstract: The present invention is related to TEX14 and germ cell intercellular bridges and compositions thereof that can be used to inhibit and/or decrease the activity and/or expression of TEX14 and/or disrupt the formation, function, and/or integrity of the intercellular bridges, including localization of key components to the intercellular bridge, for example. In particular aspects, the methods and compositions are employed for fertility and infertility applications.

Abstract: The present invention relates generally to ovary-specific genes (O1-180, O1-184 and O1-236) and the proteins they encode. Also provided are methods for detecting cell proliferative or degenerative disorders in reproductive tissues. Yet further, the invention provides methods for scrounge of compounds that interact and/or modulate the expression or activity of the ovary-specific genes. These compounds are possible contraceptive agents and/or fertility agents.

Abstract: Ovary specific proteins O1 180, O1 184 and O1 236, polynucleotides encoding them, antibodies which are immunoreactive with them and vectors and host cells containing O1 180, O1 184 or O1 236 are provided. Also provided are methods for detecting cell proliferative or degenerative disorders of ovarian origin and which are associated with O1 180, O1 184 or O1 236. Further provided are methods for the evaluation of potential contraceptives using the proteins of the invention, as well as methods for the screening for genetic mutations in signaling pathways that are associated with some forms of human infertility or gynecological cancers, also using the proteins/mRNAs/genes of the invention. The proteins/mRNAs/genes of the invention may also be used as markers for identifying primary and metastatic neoplasms of ovarian origin and as indicators of developmental anomalies in prenatal screening procedures.

Abstract: The present invention highlights the role of acetyl-CoA carboxylase through its product malonyl-CoA in regulating fatty acid oxidation and synthesis, glucose metabolism and energy homeostasis. It discloses transgenic mice with inactivating mutations in the endogenous gene for the acetyl-CoA carboxylase 2 isoform of acetyl-CoA carboxylase. Inactivation of acetyl-CoA carboxylase 2 results in mice exhibiting a phenotype of reduced malonyl-CoA levels in skeletal muscle and heart, unrestricted fat oxidation, and reduced fat accumulation in the liver and fat storage cells. As a result, the mice consume more food but accumulate less fat and remain leaner than wild-type mice fed the same diet. These results demonstrate that inhibition of ACC2 acetyl-CoA carboxylase could be used to regulate fat oxidation and accumulation for purposes of weight control.

Abstract: The present invention highlights the role of acetyl-CoA carboxylase through its product malonyl-CoA in regulating fatty acid oxidation and synthesis, glucose metabolism and energy homeostasis. It discloses transgenic mice with inactivating mutations in the endogenous gene for the acetyl-CoA carboxylase 2 isoform of acetyl-CoA carboxylase. Inactivation of acetyl-CoA carboxylase 2 results in mice exhibiting a phenotype of reduced malonyl-CoA levels in skeletal muscle and heart, unrestricted fat oxidation, and reduced fat accumulation in the liver and fat storage cells. As a result, the mice consume more food but accumulate less fat and remain leaner than wild-type mice fed the same diet. The instant invention provides a useful animal model to regulate malonyl-CoA production by ACC2 in the regulation of fatty acid oxidation by muscle, heart, liver and other tissues. They also identify potential inhibitors for studying the mechanisms of fat metabolism and weight control.

Abstract: The present invention highlights the role of acetyl-CoA carboxylase through its product malonyl-CoA in regulating fatty acid oxidation and synthesis, glucose metabolism and energy homeostasis. It discloses transgenic mice with inactivating mutations in the endogenous gene for the acetyl-CoA carboxylase 2 isoform of acetyl-CoA carboxylase. Inactivation of acetyl-CoA carboxylase 2 results in mice exhibiting a phenotype of reduced malonyl-CoA levels in skeletal muscle and heart, unrestricted fat oxidation, and reduced fat accumulation in the liver and fat storage cells. As a result, the mice consume more food but accumulate less fat and remain leaner than wild-type mice fed the same diet. These results demonstrate that inhibition of ACC2 acetyl-CoA carboxylase could be used to regulate fat oxidation and accumulation for purposes of weight control.