Abstract: The invention features a method of inhibiting formation of atherosclerotic lesions by administering to a mammal, e.g., a human patient who has been identified as suffering from or at risk of developing atherosclerosis, a compound that reduces expression or activity of AFABP.

Abstract: This invention is directed to an in vitro system for rapidly and uniformly inducing immortalized neural crest cells to differentiate to vascular smooth muscle cells. As excessive proliferation of vascular smooth muscle cells is a phenotypic response to the development of occlusive arteriosclerotic disease, the in vitro system of this invention is used to identify molecular regulators of smooth muscle cell development and differentiation. As the molecular regulators of smooth muscle cell differentiation are identified, the invention also encompasses methods to isolate the genes coding for these regulators. This invention also relates to molecules identified through the use of the invention's in vitro system, as well as to compounds that inhibit or regulate the identified molecules.

Abstract: The invention features a aortic carboxypeptidase-like polypeptide (ACLP), DNA encoding ACLP, and methods of detecting genetic alterations associated with abdominal wall defects.

Abstract: The invention features a aortic carboxypeptidase-like polypeptide (ACLP), DNA encoding ACLP, and methods of detecting genetic alterations associated with abdominal wall defects.

Abstract: The invention features a aortic carboxypeptidase-like polypeptide (ACLP), DNA encoding ACLP, and methods of detecting genetic alterations associated with abdominal wall defects.

Abstract: A method of inhibiting angiogenesis in a mammal by administering to the mammal a compound which inhibits binding of endothelial PAS domain protein-1 to cis-acting transcription regulatory sequence in the promoter region of a gene encoding an angiogenic factor.

Abstract: The invention features a method of inhibiting hypertension in a mammal by administering to the mammal a compound that reduces expression or activity of SmLIM.

Abstract: Aortic-preferentially-expressed gene-1 (APEG-1) and striated muscle preferentially expressed (SPEG) polypeptide, DNA sequences encoding and controlling the transcription of the APEG-1/SPEG encoding gene, methods of diagnosing vascular injury, methods of conferring smooth muscle-cell specific expression, and methods of inhibiting vascular smooth muscle cell proliferation by increasing the level of APEG-1 at the site of vascular injury.

Abstract: The invention features a aortic carboxypeptidase-like polypeptide (ACLP), DNA encoding ACLP, and methods of detecting genetic alterations associated with abdominal wall defects.

Abstract: Disclosed is a polypeptide termed UBCE2A that catalyzes the covalent attachment of ubiquitin to the transcription factor E2A, thereby triggering the degradation of E2A. Also disclosed are DNAs encoding UBCE2A.

Abstract: Aortic-preferentially-expressed gene-1 (APEG-1) and striated muscle preferentially expressed (SPEG) polypeptide, DNA sequences encoding and controlling the transcription of the APEG-1/SPEG encoding gene, methods of diagnosing vascular injury, methods of conferring smooth muscle-cell specific expression, and methods of inhibiting vascular smooth muscle cell proliferation by increasing the level of APEG-1 at the site of vascular injury.

Abstract: A method of inhibiting angiogenesis in a mammal by administering to the mammal a compound which inhibits binding of endothelial PAS domain protein-1 to cis-acting transcription regulatory sequence in the promoter region of a gene encoding an angiogenic factor.

Abstract: Aortic-preferentially-expressed gene-1 (APEG-1) and striated muscle preferentially expressed (SPEG) polypeptide, DNA sequences encoding and controlling the transcription of the APEG-1/SPEG encoding gene, methods of diagnosing vascular injury, methods of conferring smooth muscle-cell specific expression, and methods of inhibiting vascular smooth muscle cell proliferation by increasing the level of APEG-1 at the site of vascular injury.

Abstract: The invention provides an isolated DNA which regulates vascular smooth muscle cell-specific transcription of a polypeptide-encoding sequence to which it is operably linked

Abstract: A substantially pure DNA comprising a sequence encoding a smooth muscle cell LIM (SmLIM) polypeptide, methods of diagnosing vascular injury by detecting a decrease in SmLIM gene expression, and methods of inhibiting vascular smooth muscle cell proliferation.

Abstract: Disclosed is a novel mammalian protein designated repressor Kruppel-like factor (RKLF). RKLF is a zinc finger protein that binds to a CACCC element in DNA, thereby repressing gene transcription. An isolated DNA encoding RKLF, vectors and cells containing the DNA, and RKLF-specific antibodies are also disclosed. The RKLF DNA or protein can be introduced into the tissues of a mammal to inhibit neoplasia or hyperplasia. Also disclosed is an in vitro screening method for identifying a compound that induces RKLF gene expression.

Abstract: Disclosed is a novel mammalian protein designated repressor Kruppel-like factor (RKLF). RKLF is a zinc finger protein that binds to a CACCC element in DNA, thereby repressing gene transcription. An isolated DNA encoding RKLF, vectors and cells containing the DNA, and RKLF-specific antibodies are also disclosed. The RKLF DNA or protein can be introduced into the tissues of a mammal to inhibit neoplasia or hyperplasia. Also disclosed is an in vitro screening method for identifying a compound that induces RKLF gene expression.

Abstract: A substantially pure DNA comprising an endothelial cell-specific promoter sequence capable of directing endothelial cell-specific transcription of a polypeptide-encoding sequence or an antisense template to which it is operably linked.

Abstract: The invention features a method of inhibiting sepsis-associated hypotension in a mammal which includes the steps of identifying a mammal suffering from or at risk of developing sepsis and administering to the mammal a compound which inhibits expression of inducible heme oxygenase (HO-1). Also disclosed are screening assays useful for identifying a compound capable of inhibiting HO-1 expression or enzymatic activity.

Abstract: Aortic-preferentially-expressed gene-1 (APEG-1) and striated muscle preferentially expressed (SPEG) polypeptide, DNA sequences encoding and controlling the transcription of the APEG-1/SPEG encoding gene, methods of diagnosing vascular injury, methods of conferring smooth muscle-cell specific expression, and methods of inhibiting vascular smooth muscle cell proliferation by increasing the level of APEG-1 at the site of vascular injury.