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smooth endoplasmic reticulum is abundant in hepatocytes, whereas most cells in the body have only small amounts.
the smooth endoplasmic reticulum (smooth er) is an abundant organelle in hepatocytes, whereas most cells in the body have small amounts of smooth er.
exon 1 contains a signal sequence that localises the receptor to the endoplasmic reticulum for transport to the cell surface.
اكسون 1 يحتوي على تسلسل إشارة إلى أن localises المستقبلة إلى الشبكة الإندوبلازمية لنقلها إلى سطح الخلية.
the dlps migrate to the endoplasmic reticulum where they obtain their third, outer layer (formed by vp7 and vp4).
تستطيع الجزيئات ثنائية الطبقات dlps الهجرة إلى الشبكة الإندوبلازمية endoplasmic reticulum والتي تحصل من عندها على طبقتها الثالثة الخارجية (تصنع بواسطة vp7 و vp4).
export from the nucleus: e.g.: the ribosomes containing both rrna formed in nucleolus, and their proteins formed in rough endoplasmic reticulum.
التصدير من النواة: على سبيل المثال: الريبوسومات التي تحتوي على كل من الرنا الريباسي المتكون في النواة ، وبروتيناتها تكونت في الشبكة الإندوبلازمية الخشنة.
Ultimo aggiornamento 2022-01-12
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this ion influx then travels down the cell membranes via t-tubules and, via calcium channel complexes, leads to the release of calcium from the sarcoplasmic reticulum.
هذا التدفق ايون ثم ينتقل عبر غشاء الخلية تي عبر الأنابيب، وعبر المجمعات قناة الكالسيوم يؤدي إلى إطلاق الكالسيوم من reticulum sarcoplasmic.
Ultimo aggiornamento 2016-03-03
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ecial attention to specific molecular sites of block- ade, contributions of indirect insulin action, and the pro- posed entity of pathway-selective hepatic insulin resistance, wherein some signaling pathways downstream of the insu- lin receptor appear to retain insulin responsiveness while others manifest insulin resistance (99, 921). having described the phenomenon of insulin resistance in section iv, we proceed to examine its mechanistic basis. mechanisms of insulin resistance are most helpfully catego- rized using the molecular mediators, pathways, and net- works involved. the remainder of this review examines the experimental support for several proposed mechanisms of cellular insulin resistance using this paradigm. several lipid moieties, including diacylglycerol (dag), cer- amides, and acylcarnitines, have been implicated in the pathogenesis of liver and skeletal muscle insulin resistance (127, 561, 724). the mechanistic pathways elucidated, with varying levels of experimental support, largely run parallel to one another such that the involvement of one mediator does not preclude the involvement of another. the putative mediators, pathways, and networks involved in lipid-induced liver and muscle insulin resistance are dis- cussed in section v. a substantial literature describes cellular mechanisms for insulin resistance that are thought to be independent of lipotoxicity. these include endoplasmic reticulum stress and the unfolded protein response (481), reactive oxygen intermediates acting in various subcellular compartments (37), and substrate competition between glucose and fatty acids (397, 677). section vi examines the experimental ev- idence for involvement of each of these pathways in typical
Ultimo aggiornamento 2021-04-14
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