Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Progression of idiopathic dilated cardiomyopathy (IDCM) is marked with extensive left ventricular remodeling whose clinical manifestations and molecular basis are poorly understood. We aimed to evaluate the clinical potential of titin ligands in monitoring progression of cardiac remodeling associated with end-stage IDCM. Expression patterns of 8 mechanoptotic machinery-associated titin ligands (ANKRD1, ANKRD2, TRIM63, TRIM55, NBR1, MLP, FHL2, and TCAP) were quantitated in endomyocardial biopsies from 25 patients with advanced IDCM. When comparing NYHA disease stages, elevated ANKRD1 expression levels marked transition from NYHA < IV to NYHA IV. ANKRD1 expression levels closely correlated with systolic strain depression and short E wave deceleration time, as determined by echocardiography. On molecular level, myocardial ANKRD1 and serum adiponectin correlated with low BAX/BCL-2 ratios, indicative of antiapoptotic tissue propensity observed during the worsening of heart failure. ANKRD1 is a potential marker for cardiac remodeling and disease progression in IDCM. ANKRD1 expression correlated with reduced cardiac contractility and compliance. The association of ANKRD1 with antiapoptotic response suggests its role as myocyte survival factor during late stage heart disease, warranting further studies on ANKRD1 during end-stage heart failure.
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PMID:Induction of Ankrd1 in Dilated Cardiomyopathy Correlates with the Heart Failure Progression. 2596 Oct 10

Mood disorders, including anxiety and depression, are thought to be characterized by disrupted neuronal synapses and altered brain plasticity. The etiology is complex, involving numerous regions of the brain, comprising a multitude of neurotransmitter and neuromodulator systems. Recently, new studies on the teneurins, an evolutionary ancient family of type II transmembrane proteins have been shown to interact with latrophilins (LPHN), a similarly phylogenetically old family of adhesion G protein-coupled receptors (GPCR) forming a transsynaptic adhesion and ligand-receptor pair. Each of the four teneurin proteins contains bioactive sequences termed the teneurin C-terminal associated peptides (TCAP-1-4), which possess a number of neuromodulatory effects. The primary structures of the TCAP are most closely similar to the corticotropin-releasing factor (CRF) family of peptides. CRF has been implicated in a number of diverse mood disorders. Via an association with dystroglycans, synthetic TCAP-1 administration to both embryonic and primary hippocampal cultures induces long-term changes in neuronal structure, specifically increased neurite outgrowth, dendritic branching, and axon growth. Rodent models treated with TCAP-1 show reduced anxiety responses in the elevated plus-maze, openfield test, and acoustic startle test and inhibited CRF-mediated cocaine-seeking behaviour. Thus the teneurin/TCAP-latrophilin interaction may play a major role in the origin, development and treatment of mood disorders.
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PMID:Teneurins, TCAP, and latrophilins: roles in the etiology of mood disorders. 2812 17