Detection of full-length and truncated neurokinin-1 receptor mRNA expression in human brain regions

Lai, Jianping; Cnaan, Avital; Zhao, Huaqing; Douglas, Steven D.

doi:10.1016/j.jneumeth.2007.10.004

Cited by 31 publications

(45 citation statements)

References 29 publications

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“…We have recently applied a SYBR green-based real-time RT-PCR for quantification of fulllength and truncated NK1R mRNA in 9 regions of human brain tissues [8]. The findings suggest that the expression levels and function of the full-length NK1R are anatomic region-dependent [8]. We demonstrated that truncated NK1R has higher expression levels than that of the full-length NK1R, and that there are significant differences in expression in different brain regions [8].…”

Section: Introductionmentioning

confidence: 95%

“…The binding and signaling properties of the truncated receptor or mutants have been compared with those of the full-length receptor that is expressed in several cell systems and differences have been observed [1,[5][6][7]. We have recently applied a SYBR green-based real-time RT-PCR for quantification of fulllength and truncated NK1R mRNA in 9 regions of human brain tissues [8]. The findings suggest that the expression levels and function of the full-length NK1R are anatomic region-dependent [8].…”

Section: Introductionmentioning

confidence: 99%

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Neurokinin-1 receptor mRNA expression differences in brains of HIV-infected individuals

Douglas

Lynch

Lai

2008

Journal of the Neurological Sciences

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The neurokinin-1 receptor, a G-protein coupled receptor, is present in cells of the nervous system and the immune system. Utilizing our recently developed SYBR green-based RT-PCR, we quantified full-length and truncated NK1R mRNA expression in the cingulate cortex and cerebellum of autopsy brains from HIV-negative and -positive individuals. In the cingulate cortex, the expression of the full-length NK1R was greater in HIV-negative individuals (n=3) in comparison to HIV-positive individuals (n=21; p-value=0.026). There were no observed differences in expression of the truncated NK1R in the cingulate cortex between HIV-positive and -negative individuals. The expression of NK1R isoforms, both truncated and full-length, was similar between HIV-negative and -positive individuals in the cerebellum. It was not possible to directly relate the magnitude of NK1R expression to impairment in neuropsychological impairment in this small cohort and none of the subjects had HIV encephalopathy. These preliminary data support the concept that the full-length form of NK1R may have important significance in cognitive functions and deficiency of this isoform may be relevant in neurologic and psychiatric manifestations of neuroAIDS.

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Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Neurokinin-1 receptor mRNA expression differences in brains of HIV-infected individuals

Douglas

Lynch

Lai

2008

Journal of the Neurological Sciences

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“…A splice variant of human NK-1R has an exon 5 deletion, which yields a truncated NK-1R with 311 residues that lacks the majority of the intracellular C-tail (37). The truncated NK-1R was identified in human monocytes and macrophages (38), brain regions (cortex, cerebellum) (39) and colonic epithelial cells of colitis-associated cancer (40).…”

Section: Discussionmentioning

confidence: 99%

Difference in expression of two neurokinin-1 receptors in adenoma and carcinoma from patients that underwent radical surgery for colorectal carcinoma

Gao

Wang

2017

Oncology Letters

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Abstract. Mechanisms underlying tumor progression remain a main problem in the diagnosis and treatment of patients with tumors. The present study compared the expression of full-length neurokinin-1 receptors (fl-NK-1R) and truncated neurokinin-1 receptors (tr-NK-1R) in adenoma and carcinoma from patients with colorectal carcinoma, to explore their possible contributions in adenoma-carcinoma progression. Samples were collected immediately following colorectal carcinoma surgery. Using reverse transcription-quantitative polymerase chain reaction and immunohistochemical staining, the relative mRNA and protein levels of tr-NK-1R and fl-NK-1R were compared in adenoma and carcinoma. tr-NK-1R mRNA was significantly upregulated (1.7 fold; P=0.026) in carcinoma tissues compared with adenoma tissues, while the fl-NK-1R transcription level showed no difference (P= 0.438). No significant change was observed in the fl-NK-1R protein level in adenoma, carcinoma and peri-carcinoma tissues (P= 0.244). However, total neurokinin-1 receptor (NK-1R) protein levels in adenoma and carcinoma tissues were significantly increased compared to peri-carcinoma tissue (P= 0.026 and P= 0.007, respectively). The outcomes suggested that the increase in total NK-1R protein in adenoma and carcinoma tissues is the result of the increase in tr-NK-1R levels. The present findings indicate that tr-NK-1R serves an important role in colorectal adenoma progression, with a possible role in adenoma-carcinoma progression. Thus, tr-NK-1R may be used as a marker for diagnosing and treating patients with colorectal adenomas.

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“…However, differentiation of these cells towards a macrophage phenotype with a phorbol ester leads to the expression of both isoforms [64], which could modulate cellular activity. Different brain regions appear to exhibit different patterns of NK 1 receptor pre-mRNA alternative splicing, with expression of the truncated NK 1 receptor often being greater than that of the full-length variant [64], which could result in effects on pain perception.…”

Section: Alternative Splicing Of Gpcr In Other Pathophysiological Conmentioning

confidence: 99%

“…[59][60][61][62][63][64] Neurokinin receptor 2 Exon exclusion Impaired ligand binding and signalling [65,66] Neuropeptide S receptor (GPRA) Alternative C-terminal exons, trancation Intracellular localization of truncated isoform [67] Opioid receptors Several Various Reviewed in [68] 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 Overview of GPCRs encoded by more than one exon. In the "pre-human genome era" it was assumed that more than 90% of human GPCRs were intronless [15].…”

Section: Closing Remarksmentioning

confidence: 99%

Alternative splicing of G protein-coupled receptors: physiology and pathophysiology

Markovic

Challiss

2009

Cell. Mol. Life Sci.

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Abstract. The G protein-coupled receptors (GPCRs) are a superfamily of transmembrane receptors that have a broad distribution and can collectively recognize a diverse array of ligands. Activation or inhibition of GPCR signalling can affect many (patho)physiological processes and consequently they are a major target for existing and emerging drug therapies.A common observation has been that the pharmacological, signalling and regulatory properties of GPCRs can vary in a cell-and tissue-specific manner. Such "phenotypic" diversity might be attributable to post-translational modifications and/or association of GPCRs with accessory proteins, however, post-transcriptional mechanisms are also likely to contribute. Although, approximately 50% of GPCR genes are intronless, those that possess introns can undergo alternative splicing, generating GPCR subtype isoforms that may differ in their pharmacological, signalling and regulatory properties. In this Review we shall highlight recent research into GPCR splice-variation, and discuss the potential consequences this might have for GPCR function in health and disease.

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Detection of full-length and truncated neurokinin-1 receptor mRNA expression in human brain regions

Cited by 31 publications

References 29 publications

Neurokinin-1 receptor mRNA expression differences in brains of HIV-infected individuals

Neurokinin-1 receptor mRNA expression differences in brains of HIV-infected individuals

Difference in expression of two neurokinin-1 receptors in adenoma and carcinoma from patients that underwent radical surgery for colorectal carcinoma

Alternative splicing of G protein-coupled receptors: physiology and pathophysiology

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