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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.

Br J Pharmacol. 1999 Jan;126(1):365-71. doi: 10.1038/sj.bjp.0702291.

The prostaglandin EP4 receptor, which couples to stimulation of adenylyl cyclase, undergoes rapid agonist-induced desensitization when expressed in CHO-K1 cells. 2. Truncation of the 488-amino acid receptor at residue 350 removes the carboxy-terminal domain and abolishes desensitization. 3. To further delineate residues involved in desensitization, the receptor was truncated at position 408, 383 or 369. Receptors truncated at position 408 or 383 underwent PGE2-induced desensitization, whereas the receptor truncated at position 369 displayed sustained activity, indicating that the essential residues for desensitization lie between 370 and 383. 4. The six serines in the 14-amino acid segment between residues 370 and 383 were mutated to alanine, retaining the entire C-terminal domain. Desensitization was absent in cells expressing this mutant. 5. The results indicate involvement of serines located between 370 and 382 in rapid desensitization of the EP4 receptor.

与腺苷酸环化酶刺激偶联的前列腺素EP4受体，在CHO-K1细胞中表达时，会经历快速的激动剂诱导脱敏。2. 在第350位残基处截断488个氨基酸的受体，会去除羧基末端结构域并消除脱敏作用。3. 为了进一步确定参与脱敏的残基，受体在第408、383或369位被截断。在第408或383位截断的受体经历了PGE2诱导的脱敏，而在第369位截断的受体表现出持续活性，表明脱敏的必需残基位于370和383之间。4. 第370和383位残基之间14个氨基酸片段中的6个丝氨酸被突变为丙氨酸，保留了整个羧基末端结构域。表达该突变体的细胞中不存在脱敏现象。5. 结果表明，位于370和382之间的丝氨酸参与了EP4受体的快速脱敏。

Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.

Br J Pharmacol. 1999 Jan;126(1):365-71. doi: 10.1038/sj.bjp.0702291.

The prostaglandin EP4 receptor, which couples to stimulation of adenylyl cyclase, undergoes rapid agonist-induced desensitization when expressed in CHO-K1 cells. 2. Truncation of the 488-amino acid receptor at residue 350 removes the carboxy-terminal domain and abolishes desensitization. 3. To further delineate residues involved in desensitization, the receptor was truncated at position 408, 383 or 369. Receptors truncated at position 408 or 383 underwent PGE2-induced desensitization, whereas the receptor truncated at position 369 displayed sustained activity, indicating that the essential residues for desensitization lie between 370 and 383. 4. The six serines in the 14-amino acid segment between residues 370 and 383 were mutated to alanine, retaining the entire C-terminal domain. Desensitization was absent in cells expressing this mutant. 5. The results indicate involvement of serines located between 370 and 382 in rapid desensitization of the EP4 receptor.

与腺苷酸环化酶刺激偶联的前列腺素EP4受体，在CHO-K1细胞中表达时，会经历快速的激动剂诱导脱敏。2. 在第350位残基处截断488个氨基酸的受体，会去除羧基末端结构域并消除脱敏作用。3. 为了进一步确定参与脱敏的残基，受体在第408、383或369位被截断。在第408或383位截断的受体经历了PGE2诱导的脱敏，而在第369位截断的受体表现出持续活性，表明脱敏的必需残基位于370和383之间。4. 第370和383位残基之间14个氨基酸片段中的6个丝氨酸被突变为丙氨酸，保留了整个羧基末端结构域。表达该突变体的细胞中不存在脱敏现象。5. 结果表明，位于370和382之间的丝氨酸参与了EP4受体的快速脱敏。