Şunu aradınız:: mrna (İngilizce - Hintçe)

mai mrna chati hu
mai mrna chati hu

mai mrna chahta hu yaar
mai mrna chahta hu yaar

me mrna chahti hu in english
me mrna chahti hu in english

the mrna is then translated into protein .
इसके बाद म्ष्णा प्रोटीन में रूपांतरित हो जाता है .

mai mrna chahti hu translate in english
माई मिर्ना छत्ती हू का अंग्रेजी में अनुवाद करें

a collection of ribosomes bound to a mrna .
आरएनए से संलग्न राइबोसोम का समूह .

mrna toh mumkin nhi pr jina bhi muski lgta hai
mrna toh mumkin nhi पीआर jina भी muski lgta है

encoded genetic information in a sequence as dna , mrna
डीएनए , एमआरएनए के रूप में एक दृश्य में इनकोडिंग आनुवंशिक जानकारी ।

but the translation is essentially going from the mrna to the proteins
लेकिन अनुवाद अनिवार्य रूप से जा रहा है

the process by which mrna is decoded to form a polypeptide during the protein synthesis .
जिस प्रक्रिया के द्वारा एमआरएनए को प्रोटीन संश्लेषण के दौरान पोलीपेप्टाइड बनाने के लिये डीकोड किया जाता है

a process of synthesis of protein by ribosomes by assembling amino acid based on the sequence of mrna .
राइबोसोम द्वारा एम आरएनए अमीनो अम्ल की श्रृंखला पर आधारित प्रोटीन संश्लेषण की प्रक्रिया .

ace2 mrna expression is also found in the cerebral cortex, striatum, hypothalamus, and brainstem.
ace2 mrna प्रकटन प्रमस्तिष्क वल्कुट, स्ट्रिएटम, हाइपोथैलेमस और मस्तिष्क स्तंभ में भी पाया जाता है।

on 17 march 2020, american pharmaceutical company pfizer announced a partnership with german company biontech to jointly develop a mrna-based vaccine.
17 मार्च 2020 को, अमेरिकी दवा कंपनी फाइजर ने जर्मन कंपनी बायोएनटेक के साथ संयुक्त रूप से mrna आधारित टीका विकसित करने के लिए साझेदारी की घोषणा की।

duchenne muscular dystrophy, a severe type of muscle weakness that usually begins at an early age and worsens quickly, may soon have a new strategy of treatment through genetic regulation. there is no known cure for duchenne muscular dystrophy. treatments usually aim to control symptoms to improve quality of life. sandeep eswarappa, assistant professor indian institute of science (iisc), bengaluru one of the 21 recipients of this year’s swarnajayanti fellowship of the department of science and technology (dst), government of india proposes to supress the disease-causing premature stop codon or the genetic process that initiates these diseases. he is trying to bring about the suppression through translational readthrough, a gene regulatory principle found in humans, yeasts, bacteria and drosophila which takes place with the variation of the genetic code. prof. sandeep’s group has been developing strategies to induce translational readthrough across genetic diseases caused by non-sense mutations --a change in dna that causes a protein to terminate or end its translation earlier than expected. they were successful in achieving this in vitro in case of thalassemia and are working on other disease models. this research work has been published in the scientific journal ‘biochemistry’ recently. with the swarna jayanti fellowship, they will extend it to duchenne muscular dystrophy. if successful, this project may lead to novel therapeutics for the treatment of genetic diseases like thalassemia, duchenne muscular dystrophy, haemophilia. in case of any protein formation genetic information present in the genome is first transcribed into an mrna, which in turn is translated into a protein. protein synthesis or translation is executed by macromolecular machinery called ribosomes. ribosomes start this process at a specific location on an mrna called ‘start codon’ and terminate at a stop signal called ‘stop codon’. in case of diseases with nonsense mutations, such mutations result in premature stop signal in mrna often resulting in non-functional truncated protein. prof. sandeep eswarappa’s laboratory at iisc has shown that in certain mrnas, under certain conditions, translating ribosomes misread the stop signal and continue till they encounter another stop signal. in this translational readthrough process, a longer protein is synthesized with an extension. this extension might change the properties of the protein. the experiments carried out by his group have revealed that such long proteins can have different localization, stability and function. “the knowledge we have already gained from our experiment have opened an unexpected avenue to treat genetic diseases caused by non-sense mutations like duchenne muscular dystrophy, haemophilia and so on,” said prof. sandeep.
duchenne muscular dystrophy, a severe type of muscle weakness that usually begins at an early age and worsens quickly, may soon have a new strategy of treatment through genetic regulation. there is no known cure for duchenne muscular dystrophy. treatments usually aim to control symptoms to improve quality of life. sandeep eswarappa, assistant professor indian institute of science (iisc), bengaluru one of the 21 recipients of this year’s swarnajayanti fellowship of the department of science and technology (dst), government of india proposes to supress the disease-causing premature stop codon or the genetic process that initiates these diseases. he is trying to bring about the suppression through translational readthrough, a gene regulatory principle found in humans, yeasts, bacteria and drosophila which takes place with the variation of the genetic code. prof. sandeep’s group has been developing strategies to induce translational readthrough across genetic diseases caused by non-sense mutations --a change in dna that causes a protein to terminate or end its translation earlier than expected. they were successful in achieving this in vitro in case of thalassemia and are working on other disease models. this research work has been published in the scientific journal ‘biochemistry’ recently. with the swarna jayanti fellowship, they will extend it to duchenne muscular dystrophy. if successful, this project may lead to novel therapeutics for the treatment of genetic diseases like thalassemia, duchenne muscular dystrophy, haemophilia. in case of any protein formation genetic information present in the genome is first transcribed into an mrna, which in turn is translated into a protein. protein synthesis or translation is executed by macromolecular machinery called ribosomes. ribosomes start this process at a specific location on an mrna called ‘start codon’ and terminate at a stop signal called ‘stop codon’. in case of diseases with nonsense mutations, such mutations result in premature stop signal in mrna often resulting in non-functional truncated protein. prof. sandeep eswarappa’s laboratory at iisc has shown that in certain mrnas, under certain conditions, translating ribosomes misread the stop signal and continue till they encounter another stop signal. in this translational readthrough process, a longer protein is synthesized with an extension. this extension might change the properties of the protein. the experiments carried out by his group have revealed that such long prote “the knowledge we have already gained from our experiment have opened an unexpected avenue to treat genetic diseases caused by non-sense mutations like duchenne muscular dystrophy, haemophilia and so on,” said prof. sandeep.