Receptors & clinical investigation最新文献_第4页

The multiple signaling modalities of adhesion G protein-coupled receptor GPR126 in development. 粘附G蛋白偶联受体GPR126在发育中的多种信号传导方式。

Receptors & clinical investigation Pub Date : 2014-07-01 DOI: 10.14800/rci.79

Chinmoy Patra, Kelly R Monk, Felix B Engel

{"title":"The multiple signaling modalities of adhesion G protein-coupled receptor GPR126 in development.","authors":"Chinmoy Patra, Kelly R Monk, Felix B Engel","doi":"10.14800/rci.79","DOIUrl":"https://doi.org/10.14800/rci.79","url":null,"abstract":"The G protein-coupled receptor (GPCR) superfamily is the largest known receptor family in the human genome. Although the family of adhesion GPCRs comprises the second largest sub-family, their function is poorly understood. Here, we review the current knowledge about the adhesion GPCR family member GPR126. GPR126 possesses a signal peptide, a 7TM domain homologous to secretin-like GPCRs, a GPS motif and an extended N-terminus containing a CUB (Complement, Uegf, Bmp1) domain, a PTX (Pentraxin) domain, a hormone binding domain and 27 putative N-glycosylation sites. Knockdown and knockout experiments in zebrafish and mice have demonstrated that Gpr126 plays an essential role in neural, cardiac and ear development. In addition, genome-wide association studies have implicated variations at the GPR126 locus in obstructive pulmonary dysfunction, in scoliosis and as a determinant of trunk length and body height. Gpr126 appears to exert its function depending on the organ system via G protein- and/or N-terminus-dependent signaling. Here, we review the current knowledge about Gpr126, which, due to the variety of its functions and its multiple signaling modalities, provides a model adhesion GPCR to understand general functional concepts utilized by adhesion GPCRs.","PeriodicalId":74650,"journal":{"name":"Receptors & clinical investigation","volume":"1 3","pages":"79"},"PeriodicalIF":0.0,"publicationDate":"2014-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4258410/pdf/nihms639158.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32895805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 22

ArfGAPs: key regulators for receptor sorting. ArfGAPs:受体分选的关键调节因子。

Receptors & clinical investigation Pub Date : 2014-06-13 DOI: 10.14800/rci.158

Yoko Shiba, Paul A Randazzo

引用次数: 3

The pERK of being a target: Kinase regulation of the orphan nuclear receptor ERRγ. 成为目标的 pERK：孤儿核受体ERRγ的激酶调控。

Receptors & clinical investigation Pub Date : 2014-01-01

Rebecca B Riggins

引用次数: 0

Prostate cancer metastatic to bone has higher expression of the calcium-sensing receptor (CaSR) than primary prostate cancer. 骨转移性前列腺癌的钙敏感受体(CaSR)表达高于原发性前列腺癌。

Receptors & clinical investigation Pub Date : 2014-01-01 DOI: 10.14800/rci.270

Jie Feng, Xiaojun Xu, Bo Li, Edward Brown, Alton B Farris, Shi-Yong Sun, Jenny J Yang

{"title":"Prostate cancer metastatic to bone has higher expression of the calcium-sensing receptor (CaSR) than primary prostate cancer.","authors":"Jie Feng, Xiaojun Xu, Bo Li, Edward Brown, Alton B Farris, Shi-Yong Sun, Jenny J Yang","doi":"10.14800/rci.270","DOIUrl":"https://doi.org/10.14800/rci.270","url":null,"abstract":"The calcium-sensing receptor (CaSR) is the principal regulator of the secretion of parathyroid hormone and plays key roles in extracellular calcium (Ca2+o) homeostasis. It is also thought to participate in the development of cancer, especially bony metastases of breast and prostate cancer. However, the expression of CaSR has not been systematically analyzed in prostate cancer from patients with or without bony metastases. By comparing human prostate cancer tissue sections in microarrays, we found that the CaSR was expressed in both normal prostate and primary prostate cancer as assessed by immunohistochemistry (IHC). We used two methods to analyze the expression level of CaSR. One was the pathological score read by a pathologist, the other was the positivity% obtained from the Aperio positive pixel count algorithm. Both of the methods gave consistent results. Metastatic prostate cancer tissue obtained from bone had higher CaSR expression than primary prostate cancer (P <0.05). The expression of CaSR in primary prostate cancers of patients with metastases to tissues other than bone was not different from that in primary prostate cancer of patients with or without bony metastases (P >0.05). The expression of CaSR in cancer tissue was not associated with the stage or status of differentiation of the cancer. These results suggest that CaSR may have a role in promoting bony metastasis of prostate cancer, hence raising the possibility of reducing the risk of such metastases with CaSR-based therapeutics.","PeriodicalId":74650,"journal":{"name":"Receptors & clinical investigation","volume":"1 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459757/pdf/nihms689322.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33254353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 23

Plakophilin-2 induced EGFR phosphorylation: a focus on the intracellular activators of EGFR. Plakophilin-2诱导的EGFR磷酸化:细胞内EGFR激活因子的研究

Receptors & clinical investigation Pub Date : 2014-01-01 DOI: 10.14800/rci.485

Kei-Ichiro Arimoto, Stephanie Weng, Dong-Er Zhang

引用次数: 3

Regulation of Androgen Receptor by E3 Ubiquitin Ligases: for More or Less. E3泛素连接酶对雄激素受体的调控:多或少。

Receptors & clinical investigation Pub Date : 2014-01-01 DOI: 10.14800/rci.122

Bo Li, Wenfu Lu, Zhenbang Chen

{"title":"Regulation of Androgen Receptor by E3 Ubiquitin Ligases: for More or Less.","authors":"Bo Li, Wenfu Lu, Zhenbang Chen","doi":"10.14800/rci.122","DOIUrl":"https://doi.org/10.14800/rci.122","url":null,"abstract":"Prostate cancer (PCa) primarily depends on the dysregulations of androgen receptor (AR) signaling pathway for the initiation and growth as well as recurrence after chemotherapy [1]. Androgen deprivation therapy (ADT) effectively alleviates symptoms of the malignancy to arrest further growth of primary tumors or progression of metastasis in patients with advanced PCa. However, relapse occurs in many patients after a short period, and PCa cells eventually become insensitive to ADT - termed castration resistant prostate cancer (CRPC) [2, 3]. Tremendous advancements have been achieved to decipher the mechanisms on AR signaling, and the ubiquitination machinery contributes to PCa directly or indirectly by either promotion of AR transcriptional activity or degradation of AR protein levels. The recent report reveals that SKP2 regulates AR protein through ubiquitin-mediated proteasomal degradation, highlighting the role of SKP2 in AR signaling. Given the pivotal roles of AKT and SKP2 in cancers, the differential mechanisms of AR ubiquitination by various E3 ligases hold valuable significance and beneficial implications for PCa control.","PeriodicalId":74650,"journal":{"name":"Receptors & clinical investigation","volume":"1 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4139040/pdf/nihms614883.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32610942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 31

Fibronectin signaling via toll-like receptprs: a novel paradigm for persistent fibrosis in scleroderma. 通过收费样受体的纤连蛋白信号传导：硬皮病持续纤维化的新范例。

Receptors & clinical investigation Pub Date : 2014-01-01 Epub Date: 2014-08-13

Swati Bhattacharyya, John Varga

引用次数: 0

Beta-2-Adrenergic Receptor Methylation Influences Asthma Phenotype in The School Inner City Asthma Study. β -2-肾上腺素能受体甲基化影响学校哮喘研究中的哮喘表型。

Receptors & clinical investigation Pub Date : 2014-01-01 DOI: 10.14800/rci.15

Jonathan M Gaffin, Wanda Phipatanakul

引用次数: 6

Role of protease-activated receptors 2 (PAR2) in ocular infections and inflammation. 蛋白酶激活受体2 (PAR2)在眼部感染和炎症中的作用。

Receptors & clinical investigation Pub Date : 2014-01-01 DOI: 10.14800/rci.291

Trivendra Tripathi, Hassan Alizadeh

{"title":"Role of protease-activated receptors 2 (PAR2) in ocular infections and inflammation.","authors":"Trivendra Tripathi, Hassan Alizadeh","doi":"10.14800/rci.291","DOIUrl":"https://doi.org/10.14800/rci.291","url":null,"abstract":"Protease-activated receptors (PARs) belong to a unique family of G protein-coupled receptors (GPCRs) that are cleaved at an activation site within the N-terminal exodomain by a variety of proteinases, essentially of the serine (Ser) proteinase family. After cleavage, the new N-terminal sequence functions as a tethered ligand, which binds intramolecularly to activate the receptor and initiate signaling. Cell signals induced through the activation of PARs appear to play a significant role in innate and adoptive immune responses of the cornea, which is constantly exposed to proteinases under physiological or pathophysiological conditions. Activation of PARs interferes with all aspects of the corneal physiology such as barrier function, transports, innate and adoptive immune responses, and functions of corneal nerves. It is not known whether the proteinase released from the microorganism can activate PARs and triggers the inflammatory responses. The role of PAR2 expressed by the corneal epithelial cells and activation by serine protease released from microorganism is discussed here. Recent evidences suggest that activation of PAR2, by the serine proteinases, play an important role in innate and inflammatory responses of the corneal infection.","PeriodicalId":74650,"journal":{"name":"Receptors & clinical investigation","volume":"1 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14800/rci.291","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33393434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Estrogen receptor-α signaling and localization regulates autophagy and unfolded protein response activation in ER+ breast cancer. 雌激素受体-α信号传导和定位调节雌激素受体阳性乳腺癌的自噬和未折叠蛋白反应激活。

Receptors & clinical investigation Pub Date : 2014-01-01 DOI: 10.14800/rci.316

Katherine L Cook, Robert Clarke

{"title":"Estrogen receptor-α signaling and localization regulates autophagy and unfolded protein response activation in ER+ breast cancer.","authors":"Katherine L Cook, Robert Clarke","doi":"10.14800/rci.316","DOIUrl":"https://doi.org/10.14800/rci.316","url":null,"abstract":"Antiestrogen therapy is commonly used to treat estrogen receptor (ER)+ breast cancers but acquired and de novo resistance limits their overall curative potential. An endoplasmic reticulum stress pathway, the unfolded protein response, and autophagy are both implicated in the development of antiestrogen therapy resistance in estrogen receptor-α (ER) positive breast cancer. Thus, we recently investigated how ERα can regulate autophagy and the unfolded protein response (Cook et al., FASEBJ, 2014). We showed that inhibiting ERα signaling stimulates autophagosome formation and flux. Moreover, we showed that ERα knockdown inhibited the unfolded protein response (UPR) signaling components. Here we support and extend this recent report showing additional data on ERα localization and provide a schematic of the overall signaling implicated by our results. Differential activation of UPR and autophagy highlight the pivotal role of ERα in regulating pro-survival signaling in breast cancer through UPR and autophagy. Furthermore, these data suggest new approaches to successful targeting ERα and preventing the regulation of key pro-survival signaling that confers resistance to endocrine therapies.","PeriodicalId":74650,"journal":{"name":"Receptors & clinical investigation","volume":"1 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4440691/pdf/nihms689324.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33331089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10