Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intervertebral disk disease is a common clinical disorder manifested by pain, ataxia, paresis, motor paralysis, and sensorimotor paralysis. The clinical features, diagnosis, and treatment of cervical and thoracolumbar disk disease have been unclear until now. In this study, some differentially expressed genes were identified, and a network was constructed based on these genes. Through the statistical analysis of nodes and the contrast of 2 more connectivity nodes, it was found that the nodes in the network are in an important position and play key roles. Several of these genes, including MAP2K6, MAP2K3, and MAPK14, belong to the MAP kinase family, and several genes, including RHOBTB2, RHOQ, and RHOH, belong to the RHO family. Therefore, we hypothesize that the development of intervertebral disk disease is related to MAP and RHO family proteins.
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PMID:Analysis of intervertebral disc-related genes. 2473 28

Gastrointestinal motility disorders (GMDs) are attributed to loss of interstitial cells of Cajal (ICC), whose survival and function are deeply dependent on the activation of KIT/SCF signalling. Based on the facts that gastrointestinal distention is common in GMD patients and SCF produced by smooth muscle cells (SMCs) is usually decreased before ICC loss, we considered a possible contribution of persistent gastrointestinal distention/stretch to SCF deficiency. In this study, chronic colonic distention mouse model, diabetic gastrointestinal paresis mouse model, cultured mouse colonic SMCs and colon specimens from Hirschsprung's disease patients were used. The results showed that SCF was clearly decreased in distent colon of mice and patients, and microRNA array and real-time PCR indicated a concomitant increase of miR-34c in distent colon. A negative regulation of miR-34c on SCF expression was confirmed by luciferase reporter assays together with knock-down and overexpression of miR-34c in cultured colonic SMCs. Using EMSA and ChIP assays, we further consolidated that in response to persistent stretch, the transcription factor AP-1/c-Jun was highly activated in colonic SMCs and significantly promoted miR-34c transcription by binding to miR-34c promoter. Knock-down or overexpression of AP-1/c-Jun in cultured colonic SMCs leads to down- or up-regulation of miR-34c, respectively. In addition, the activation of AP-1/c-Jun was through ERK1/2 signalling provoked by Ca2+ overload in colonic SMCs that were subject to persistent stretch. In conclusion, our data demonstrated that persistent distention/stretch on colonic SMCs could suppress SCF production probably through Ca2+ -ERK-AP-1-miR-34c deregulation, resulting in ICC loss or impairment and GMD progress.
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PMID:Persistent distention of colon damages interstitial cells of Cajal through Ca2+ -ERK-AP-1-miR-34c-SCF deregulation. 2858 Jul 75