Relax its just life @discoveringpmadupe - Tumblr Blog

Spring, in Cape st. Francis

#love #coolaf #naturalhair coolaf magical black girl #gold #phdlife #blue skies

Egon Schiele, femme assise de dos avec bas noirs et une ligne rouge, 1914. Musée Leopold, Vienne

“I didn’t want to be around it. I didn’t want to hear the yelling, or the fighting. So I ran away from the badness. I spent my childhood at the houses of friends. I surrounded myself with people. And I became a social butterfly. Even when I moved to London ten years ago, I still kept my old friends around me. There were always so many people coming and going. But then we all turned thirty, and suddenly everyone was going, and not coming back again. Things began to fall apart for me. I lost my support network. I lost my job. I found myself in an abusive relationship, just like my mother had been. I was so angry at myself for going through the same cycle. But I allowed it to happen, because he was the only thing keeping me from being completely alone. But one day I did it. I finally left him. For a moment I had no friends, no job, no place to live, and no relationship. I wanted to run back home. But I stayed in London. I stayed just to teach myself that I could be ok. I rented a room in a house full of strangers. I began doing things on my own. I went to a music festival by myself, and ended up meeting the best friends of my life. I stayed single for three good years. I taught myself what I want and what I deserve. Now I’ve got a great boyfriend who’s not insecure, who’s not jealous, who’s not controlling, who lets me be myself. And I’ve learned that I’m independent. Growing up I always thought of myself as independent. But it was just a thought. I never knew. But now I know.” (London, England)

Spring has sprung.

#naturalhair coolaf magical black girl #love #coolaf #spring #gold #phdlife

thelatestkate

August 2019 Illustrations ヽ(• ‿•)ノ

discoveringpmadupe

The retrogene UTP14c, involved in human male infertility, ovarian cancer and the best way of studying it.

By; Palesa P. Madupe

Literature survey So where does it all begin? Retrogenes, processed pseudogenes (PP) and pseudogenes are abundant in the human genome and most of their function was unknown up until recently (until the human genome project). They are mostly involved in disease development in humans, like in the case of myosin light chain kinase pseudogene which has been documented to be highly expressed in cancer cells (1). Pseudogenes are dysfunctional genomic loci with sequence similarity to functional genes but lacking coding potential due to the presence of disruptive mutations such as frame shifts and premature stop codons (2) . Pseudogenes are described into different categories; processed pseudogenes which are created via retrotranspositioning of mRNA from functional protein coding loci back into the genome, or duplicated unprocessed pseudogenes derived from duplication of functional genes or unitary pseudogenes, which arises through in situ mutations in previously functional protein coding genes (3) . Retrogenes are born via the reverse transcription of mature messenger RNA (mRNA) from parental genes and thus have no introns (mRNA sequence that can be converted into proteins) (4). They contain 3’ end poly A tail and are flanked by short directed repeats. They arise from transposable elements, defined as DNA sequences that have the ability to integrate into the genome at a new locus within the same cell. These elements contain DNA transposons and retrotransposons. Retrotransposons can be RNA that is reverse transcribed into DNA and then integrated into the genome at a new location (4). The original transposon is maintained in situ therefore it duplicates itself within the same cell; referred to as copy and paste method. Retrotransposons are devised into 2 classed based on the presence or absence of long terminal repeats (LTR). Those that contain LTRs are like retroviruses they contain them at both ends of the strand. The non-LTR have the 3’end poly A tails (5). The vast majority of retrotransposed copies of mRNA are inactivated into PP. It is only in a few cases that they evolve into new genes, ie. Retrogenes which can be transcribed and translated in to proteins. Like in the case of UTP14c gene; which is involved in 18S rRNA synthesis (the small subunit of the eukaryotic cytoplasmic ribosomes, which is essential in eukaryotic cells). The retrotransposed copy of the source gene is integrated into the 3’ un-translated region last exon of a glycerol transferase-containing gene (GT8). The 3’part of the exon 3 and the whole intron 3 and exon 4 of the GT8 gene are enlisted with unchanged exon-intron structure, to form a single intron containing UTP14c. This makes the exon segments of GT8 un translated (6). The source gene UTP14c is a ubiquitously expressed X-linked gene. In mouse; its retrogene UTP14b is expressed in the male germ cells and when its mutated it results in early spermatogenic arrest and male infertility (7). Humans have the strict ortholog of UTP14b in the synthetic region of chromosome 2, and it has degenerated and its no longer functional (it has become a PP). A second retrogene is found in chromosome 13 which is expressed in testis and ovaries the function has been documented to be equivalent to that of mouse UTP14b (6,8). The UTP14 protein has been predicted to be part of the small subunit processome complex that binds to U3 small nucleolar RNA involved in the synthesis of the 18S rRNA (9). The UTP14c gene has acquired specific promoter/enhancer elements, thus this restricts the activity of the gene in the ovaries and testis. The data machinery that is found in the germ cells is different from that is found in the somatic cells. Because the UTP14c gene is incorporated into the GT8 gene, this makes its production bypassed. The polyadenylation signal of the gene GT8 is lost (6). Mutations that occur within the UTP14c gene have shown to lead to early maturation arrest in the formation off sperm cells. The mutations lead to the protein of UTP14c gene not being able to form the protein complex of the synthesis of 18S rRNA. UTP14c is expressed in 50% of normal human ovaries and 80% of ovaries that have cancer (ovarian cancer). It was documented to down regulate tumour protein 53 (TP53) in both the nucleus and cytoplasm by targeting it for proteolytic degradation. This prevents the cancer cells expressing UTP14c from entering the apoptotic pathway. The loss of TP53 down regulates micro RNA-154 (miRNA-154) expression. This then activates factors that promote oncogenesis and cellular pluripotency which can develop ovarian cancer. How does expression of UTP14c actually disrupt the TP53 pathway? The TP53 regulates the expression of mi-RNA154, it binds to the promoter region of mi-RNA-154 and its up regulates the pre RNA synthesis of mi-RNA 154. It also bind to the muclear RNAse 3 drosha which stimulates the processing of the mi-RNA 154 pre- RNA into the mature version. The biological active form of mi-RNA 154 acts as an anti-tumorigenic factor blocking the expression of c-myc, cell reprogramming gene and the cells proliferation/invasion gene muc1 (6) . So how would we better study, UTP14c retrogene? A little bit of history Recombinant DNA technology (10) has changed how we understand the functioning of genes, proteins and nucleic acid. Recombinant DNA technology refers to making of new combinations of DNA fragments which are not found existing together in nature. The isolation of the desired DNA segments allows for exact DNA analysis, and practical application in medicine like drug discovery, in agriculture like the creation of bio-control agents and in industrial application production of food additives. Here is an oversimplified way of making recombinant DNA; isolate DNA from whatever source, cut with restriction enzymes, ligate (essentially paste) into cloning vector, then transform the recombinant DNA molecule into host cell, grow the host. Each cell from then onwards will carry the desired recombinant DNA molecule. Each of the steps mentioned here have intrinsic and extrinsic factors to them and their not as plain as mentioned. To further study the recombinant DNA molecule, depends on what the researcher is interested in. To determine the function of the recombinant DNA molecule one can conduct a site generated mutagenesis, the recombinant DNA fragment may be changed by changing a base in the primer sequence, for the polymerase chain reaction (PCR) of the cloned DNA molecule. During the PCR the amplicons generated will contain the mutation selected for by the researcher (11). Because of the generated site mutation the gene produce for that DNA fragment might not function like the wild type gene, thus one can then extrapolate that a mutation at position X leads to noticeable missing functions. More recently we have seen outbreaks of the combination of recombinant DNA technology and nanoscience. Nanoscience refers to the science; manipulation and the development of chemical and biological structure that are on the scale of single atoms. Like in the production of antibodies, this technology is been used to manufacture antibodies that have very high affinity to specific substrates. The problem has been a way of delivering these antibodies to that specific site. Ingestion would lead to the immune system attacking them. The attachment of these recombinant antibodies to carbon nanotubes with radio or fluorescent labelling, can directly deliver antibodies directly where their required (12). Recombinant DNA technology has also advanced the study of protein function and drug design. Knowing the three-dimensional (3-D) structure of a protein has enable the determination of the active site (where substrates bind) in vivo. Knowing the active sites of protein and enzyme has enabled drug design to be more effective (13). The 3-D structure of proteins can be determined via nuclear magnetic resonance (NMR) spectroscopy, which is able to reveal atomic structures of macromolecules in solution. NMR relies on the fact that atomic nuclei are magnetic. The purified protein in solution is then placed in a strong magnetic field and probed with radio waves. A distinct resonance is observed and that can be analysed to give a list of atomic nuclei that are close to one another, and to characterise the local conformation of atoms that are bonded together. All these specifications are used to a model a protein (14). Protein X-ray crystallography, it’s the determination of the 3-D structure of biological macromolecules using diffraction technology on a single crystal. This technique is much better than NMR because X-ray crystallography gives a better/ high resolution. The first protein crystal structure was of myoglobin in the year 1932 by Theorell A, the resolution of the protein was 6 Å (Angstron). Resolution measures the amount and level of details present in the protein. High resolution structure are those that have very low Angstron values

The retrogene UTP14c, involved in human male infertility, ovarian cancer and the best way of studying it.

By; Palesa P. Madupe Literature survey So where does it all begin? Retrogenes, processed pseudogenes (PP) and pseudogenes are abundant in the human genome and most of their function was unknown up until recently (until the human genome project). They are mostly involved in disease development in humans, like in the case of myosin light chain kinase pseudogene which has been documented to be highly expressed in cancer cells (1). Pseudogenes are dysfunctional genomic loci with sequence similarity to functional genes but lacking coding potential due to the presence of disruptive mutations such as frame shifts and premature stop codons (2) . Pseudogenes are described into different categories; processed pseudogenes which are created via retrotranspositioning of mRNA from functional protein coding loci back into the genome, or duplicated unprocessed pseudogenes derived from duplication of functional genes or unitary pseudogenes, which arises through in situ mutations in previously functional protein coding genes (3) . Retrogenes are born via the reverse transcription of mature messenger RNA (mRNA) from parental genes and thus have no introns (mRNA sequence that can be converted into proteins) (4). They contain 3’ end poly A tail and are flanked by short directed repeats. They arise from transposable elements, defined as DNA sequences that have the ability to integrate into the genome at a new locus within the same cell. These elements contain DNA transposons and retrotransposons. Retrotransposons can be RNA that is reverse transcribed into DNA and then integrated into the genome at a new location (4). The original transposon is maintained in situ therefore it duplicates itself within the same cell; referred to as copy and paste method. Retrotransposons are devised into 2 classed based on the presence or absence of long terminal repeats (LTR). Those that contain LTRs are like retroviruses they contain them at both ends of the strand. The non-LTR have the 3’end poly A tails (5). The vast majority of retrotransposed copies of mRNA are inactivated into PP. It is only in a few cases that they evolve into new genes, ie. Retrogenes which can be transcribed and translated in to proteins. Like in the case of UTP14c gene; which is involved in 18S rRNA synthesis (the small subunit of the eukaryotic cytoplasmic ribosomes, which is essential in eukaryotic cells). The retrotransposed copy of the source gene is integrated into the 3’ un-translated region last exon of a glycerol transferase-containing gene (GT8). The 3’part of the exon 3 and the whole intron 3 and exon 4 of the GT8 gene are enlisted with unchanged exon-intron structure, to form a single intron containing UTP14c. This makes the exon segments of GT8 un translated (6). The source gene UTP14c is a ubiquitously expressed X-linked gene. In mouse; its retrogene UTP14b is expressed in the male germ cells and when its mutated it results in early spermatogenic arrest and male infertility (7). Humans have the strict ortholog of UTP14b in the synthetic region of chromosome 2, and it has degenerated and its no longer functional (it has become a PP). A second retrogene is found in chromosome 13 which is expressed in testis and ovaries the function has been documented to be equivalent to that of mouse UTP14b (6,8). The UTP14 protein has been predicted to be part of the small subunit processome complex that binds to U3 small nucleolar RNA involved in the synthesis of the 18S rRNA (9). The UTP14c gene has acquired specific promoter/enhancer elements, thus this restricts the activity of the gene in the ovaries and testis. The data machinery that is found in the germ cells is different from that is found in the somatic cells. Because the UTP14c gene is incorporated into the GT8 gene, this makes its production bypassed. The polyadenylation signal of the gene GT8 is lost (6). Mutations that occur within the UTP14c gene have shown to lead to early maturation arrest in the formation off sperm cells. The mutations lead to the protein of UTP14c gene not being able to form the protein complex of the synthesis of 18S rRNA. UTP14c is expressed in 50% of normal human ovaries and 80% of ovaries that have cancer (ovarian cancer). It was documented to down regulate tumour protein 53 (TP53) in both the nucleus and cytoplasm by targeting it for proteolytic degradation. This prevents the cancer cells expressing UTP14c from entering the apoptotic pathway. The loss of TP53 down regulates micro RNA-154 (miRNA-154) expression. This then activates factors that promote oncogenesis and cellular pluripotency which can develop ovarian cancer. How does expression of UTP14c actually disrupt the TP53 pathway? The TP53 regulates the expression of mi-RNA154, it binds to the promoter region of mi-RNA-154 and its up regulates the pre RNA synthesis of mi-RNA 154. It also bind to the muclear RNAse 3 drosha which stimulates the processing of the mi-RNA 154 pre- RNA into the mature version. The biological active form of mi-RNA 154 acts as an anti-tumorigenic factor blocking the expression of c-myc, cell reprogramming gene and the cells proliferation/invasion gene muc1 (6) . So how would we better study, UTP14c retrogene? A little bit of history Recombinant DNA technology (10) has changed how we understand the functioning of genes, proteins and nucleic acid. Recombinant DNA technology refers to making of new combinations of DNA fragments which are not found existing together in nature. The isolation of the desired DNA segments allows for exact DNA analysis, and practical application in medicine like drug discovery, in agriculture like the creation of bio-control agents and in industrial application production of food additives. Here is an oversimplified way of making recombinant DNA; isolate DNA from whatever source, cut with restriction enzymes, ligate (essentially paste) into cloning vector, then transform the recombinant DNA molecule into host cell, grow the host. Each cell from then onwards will carry the desired recombinant DNA molecule. Each of the steps mentioned here have intrinsic and extrinsic factors to them and their not as plain as mentioned. To further study the recombinant DNA molecule, depends on what the researcher is interested in. To determine the function of the recombinant DNA molecule one can conduct a site generated mutagenesis, the recombinant DNA fragment may be changed by changing a base in the primer sequence, for the polymerase chain reaction (PCR) of the cloned DNA molecule. During the PCR the amplicons generated will contain the mutation selected for by the researcher (11). Because of the generated site mutation the gene produce for that DNA fragment might not function like the wild type gene, thus one can then extrapolate that a mutation at position X leads to noticeable missing functions. More recently we have seen outbreaks of the combination of recombinant DNA technology and nanoscience. Nanoscience refers to the science; manipulation and the development of chemical and biological structure that are on the scale of single atoms. Like in the production of antibodies, this technology is been used to manufacture antibodies that have very high affinity to specific substrates. The problem has been a way of delivering these antibodies to that specific site. Ingestion would lead to the immune system attacking them. The attachment of these recombinant antibodies to carbon nanotubes with radio or fluorescent labelling, can directly deliver antibodies directly where their required (12). Recombinant DNA technology has also advanced the study of protein function and drug design. Knowing the three-dimensional (3-D) structure of a protein has enable the determination of the active site (where substrates bind) in vivo. Knowing the active sites of protein and enzyme has enabled drug design to be more effective (13). The 3-D structure of proteins can be determined via nuclear magnetic resonance (NMR) spectroscopy, which is able to reveal atomic structures of macromolecules in solution. NMR relies on the fact that atomic nuclei are magnetic. The purified protein in solution is then placed in a strong magnetic field and probed with radio waves. A distinct resonance is observed and that can be analysed to give a list of atomic nuclei that are close to one another, and to characterise the local conformation of atoms that are bonded together. All these specifications are used to a model a protein (14). Protein X-ray crystallography, it’s the determination of the 3-D structure of biological macromolecules using diffraction technology on a single crystal. This technique is much better than NMR because X-ray crystallography gives a better/ high resolution. The first protein crystal structure was of myoglobin in the year 1932 by Theorell A, the resolution of the protein was 6 Å (Angstron). Resolution measures the amount and level of details present in the protein. High resolution structure are those that have very low Angstron values < 2 Å. For this method the protein is purified and crystallised and the hit with intense beam of X-rays. The diffraction is measured and then analysed to determine the distribution of electrons in the protein (15). X-ray crystallography provides detailed atomic information, showing every atom in the protein together with atomic details of ligands, inhibitors, ions, and other molecules that incorporated in the protein. With the backdrop of this information the best way of understanding the structure and function of the UTP14 protein is via recombinant DNA technology and X-ray crystallography, especially if we want to eventually design a drug that can be used in fighting the cancer and infertility that is caused by the UTP14c gene. Citations 1. Han YJ, Ma SF, Yourek G, Park Y-D, Garcia JGN. A transcribed pseudogene of MYLK promotes cell proliferation . FASEB J. 2011; 2. Mighell AJ, Smith NR, Robinson PA, Markham AF. Vertebrate pseudogenes. FEBS Lett. 2000; 3. Harrison PM, Zheng D, Zhang Z, Carriero N, Gerstein M. Transcribed processed pseudogenes in the human genome: An intermediate form of expressed retrosequence lacking protein-coding ability. Nucleic Acids Res. 2005; 4. Kaessmann H, Vinckenbosch N, Long M. RNA-based gene duplication: Mechanistic and evolutionary insights. Nature Reviews Genetics. 2009. 5. Ding W, Lin L, Chen B, Dai J. L1 elements, processed pseudogenes and retrogenes in mammalian genomes. IUBMB Life. 2006. 6. Rohozinski J, Lamb DJ, Bishop CE. UTP14c Is a Recently Acquired Retrogene Associated with Spermatogenesis and Fertility in Man1. Biol Reprod. 2005; 7. Boettger-Tong HL, Johnston DS, Russell LD, Griswold MD, Bishop CE. Juvenile Spermatogonial Depletion (jsd) Mutant Seminiferous Tubules Are Capable of Supporting Transplanted Spermatogenesis1. Biol Reprod. 2005; 8. Bradley J, Baltus A, Skaletsky H, Royce-Tolland M, Dewar K, Page DC. An X-to-autosome retrogene is required for spermatogenesis in mice. Nat Genet. 2004; 9. Dragon F, Gallagher JEG, Compagnone-Post PA, Mitchell BM, Porwancher KA, Wehner KA, et al. A large nucleolar U3 ribonucleoprotein required for 18S ribosomal RNA biogenesis. Nature. 2002; 10. Cohen SN, Chang AC, Hsu L. Nonchromosomal antibiotic resistance in bacteria: genetic transformation of Escherichia coli by R-factor DNA. Proc Natl Acad Sci U S A. 1972; 11. Hemsley A, Arnheim N, Toney MD, Cortopassi G, Galas DJ. A simple method for site-directed mutagenesis using the polymerase chain reaction. Nucleic Acids Research. 1989. 12. McDevitt MR, Chattopadhyay D, Kappel BJ, Jaggi JS, Schiffman SR, Antczak C, et al. Tumor Targeting with Antibody-Functionalized, Radiolabeled Carbon Nanotubes. J Nucl Med. 2007; 13. Verlinde CL, Hol WG. Structure-based drug design: progress, results and challenges. Structure. 1994; 14. Wüthrich K. The way to NMR structures of proteins. Nat Struct Biol. 2001; 15. Wlodawer A, Minor W, Dauter Z, Jaskolski M. Protein crystallography for aspiring crystallographers or how to avoid pitfalls and traps in macromolecular structure determination. FEBS J. 2013;

nucleicacidbased

The retrogene UTP14c, involved in human male infertility, ovarian cancer and the best way of studying it.

By; Palesa P. Madupe

Literature survey So where does it all begin? Retrogenes, processed pseudogenes (PP) and pseudogenes are abundant in the human genome and most of their function was unknown up until recently (until the human genome project). They are mostly involved in disease development in humans, like in the case of myosin light chain kinase pseudogene which has been documented to be highly expressed in cancer cells (1). Pseudogenes are dysfunctional genomic loci with sequence similarity to functional genes but lacking coding potential due to the presence of disruptive mutations such as frame shifts and premature stop codons (2) . Pseudogenes are described into different categories; processed pseudogenes which are created via retrotranspositioning of mRNA from functional protein coding loci back into the genome, or duplicated unprocessed pseudogenes derived from duplication of functional genes or unitary pseudogenes, which arises through in situ mutations in previously functional protein coding genes (3) . Retrogenes are born via the reverse transcription of mature messenger RNA (mRNA) from parental genes and thus have no introns (mRNA sequence that can be converted into proteins) (4). They contain 3’ end poly A tail and are flanked by short directed repeats. They arise from transposable elements, defined as DNA sequences that have the ability to integrate into the genome at a new locus within the same cell. These elements contain DNA transposons and retrotransposons. Retrotransposons can be RNA that is reverse transcribed into DNA and then integrated into the genome at a new location (4). The original transposon is maintained in situ therefore it duplicates itself within the same cell; referred to as copy and paste method. Retrotransposons are devised into 2 classed based on the presence or absence of long terminal repeats (LTR). Those that contain LTRs are like retroviruses they contain them at both ends of the strand. The non-LTR have the 3’end poly A tails (5). The vast majority of retrotransposed copies of mRNA are inactivated into PP. It is only in a few cases that they evolve into new genes, ie. Retrogenes which can be transcribed and translated in to proteins. Like in the case of UTP14c gene; which is involved in 18S rRNA synthesis (the small subunit of the eukaryotic cytoplasmic ribosomes, which is essential in eukaryotic cells). The retrotransposed copy of the source gene is integrated into the 3’ un-translated region last exon of a glycerol transferase-containing gene (GT8). The 3’part of the exon 3 and the whole intron 3 and exon 4 of the GT8 gene are enlisted with unchanged exon-intron structure, to form a single intron containing UTP14c. This makes the exon segments of GT8 un translated (6). The source gene UTP14c is a ubiquitously expressed X-linked gene. In mouse; its retrogene UTP14b is expressed in the male germ cells and when its mutated it results in early spermatogenic arrest and male infertility (7). Humans have the strict ortholog of UTP14b in the synthetic region of chromosome 2, and it has degenerated and its no longer functional (it has become a PP). A second retrogene is found in chromosome 13 which is expressed in testis and ovaries the function has been documented to be equivalent to that of mouse UTP14b (6,8). The UTP14 protein has been predicted to be part of the small subunit processome complex that binds to U3 small nucleolar RNA involved in the synthesis of the 18S rRNA (9). The UTP14c gene has acquired specific promoter/enhancer elements, thus this restricts the activity of the gene in the ovaries and testis. The data machinery that is found in the germ cells is different from that is found in the somatic cells. Because the UTP14c gene is incorporated into the GT8 gene, this makes its production bypassed. The polyadenylation signal of the gene GT8 is lost (6). Mutations that occur within the UTP14c gene have shown to lead to early maturation arrest in the formation off sperm cells. The mutations lead to the protein of UTP14c gene not being able to form the protein complex of the synthesis of 18S rRNA. UTP14c is expressed in 50% of normal human ovaries and 80% of ovaries that have cancer (ovarian cancer). It was documented to down regulate tumour protein 53 (TP53) in both the nucleus and cytoplasm by targeting it for proteolytic degradation. This prevents the cancer cells expressing UTP14c from entering the apoptotic pathway. The loss of TP53 down regulates micro RNA-154 (miRNA-154) expression. This then activates factors that promote oncogenesis and cellular pluripotency which can develop ovarian cancer. How does expression of UTP14c actually disrupt the TP53 pathway? The TP53 regulates the expression of mi-RNA154, it binds to the promoter region of mi-RNA-154 and its up regulates the pre RNA synthesis of mi-RNA 154. It also bind to the muclear RNAse 3 drosha which stimulates the processing of the mi-RNA 154 pre- RNA into the mature version. The biological active form of mi-RNA 154 acts as an anti-tumorigenic factor blocking the expression of c-myc, cell reprogramming gene and the cells proliferation/invasion gene muc1 (6) . So how would we better study, UTP14c retrogene? A little bit of history Recombinant DNA technology (10) has changed how we understand the functioning of genes, proteins and nucleic acid. Recombinant DNA technology refers to making of new combinations of DNA fragments which are not found existing together in nature. The isolation of the desired DNA segments allows for exact DNA analysis, and practical application in medicine like drug discovery, in agriculture like the creation of bio-control agents and in industrial application production of food additives. Here is an oversimplified way of making recombinant DNA; isolate DNA from whatever source, cut with restriction enzymes, ligate (essentially paste) into cloning vector, then transform the recombinant DNA molecule into host cell, grow the host. Each cell from then onwards will carry the desired recombinant DNA molecule. Each of the steps mentioned here have intrinsic and extrinsic factors to them and their not as plain as mentioned. To further study the recombinant DNA molecule, depends on what the researcher is interested in. To determine the function of the recombinant DNA molecule one can conduct a site generated mutagenesis, the recombinant DNA fragment may be changed by changing a base in the primer sequence, for the polymerase chain reaction (PCR) of the cloned DNA molecule. During the PCR the amplicons generated will contain the mutation selected for by the researcher (11). Because of the generated site mutation the gene produce for that DNA fragment might not function like the wild type gene, thus one can then extrapolate that a mutation at position X leads to noticeable missing functions. More recently we have seen outbreaks of the combination of recombinant DNA technology and nanoscience. Nanoscience refers to the science; manipulation and the development of chemical and biological structure that are on the scale of single atoms. Like in the production of antibodies, this technology is been used to manufacture antibodies that have very high affinity to specific substrates. The problem has been a way of delivering these antibodies to that specific site. Ingestion would lead to the immune system attacking them. The attachment of these recombinant antibodies to carbon nanotubes with radio or fluorescent labelling, can directly deliver antibodies directly where their required (12). Recombinant DNA technology has also advanced the study of protein function and drug design. Knowing the three-dimensional (3-D) structure of a protein has enable the determination of the active site (where substrates bind) in vivo. Knowing the active sites of protein and enzyme has enabled drug design to be more effective (13). The 3-D structure of proteins can be determined via nuclear magnetic resonance (NMR) spectroscopy, which is able to reveal atomic structures of macromolecules in solution. NMR relies on the fact that atomic nuclei are magnetic. The purified protein in solution is then placed in a strong magnetic field and probed with radio waves. A distinct resonance is observed and that can be analysed to give a list of atomic nuclei that are close to one another, and to characterise the local conformation of atoms that are bonded together. All these specifications are used to a model a protein (14). Protein X-ray crystallography, it’s the determination of the 3-D structure of biological macromolecules using diffraction technology on a single crystal. This technique is much better than NMR because X-ray crystallography gives a better/ high resolution. The first protein crystal structure was of myoglobin in the year 1932 by Theorell A, the resolution of the protein was 6 Å (Angstron). Resolution measures the amount and level of details present in the protein. High resolution structure are those that have very low Angstron values

Summer gold ☀️

#love #gold #naturalhair coolaf magical black girl #coolaf #summer

end0skeletal

This September (2018) in Aitoliko, Greece, the beach was covered in a blanket of massive spiderwebs.

According to Maria Chatzaki, an associate professor in the Department of Molecular Biology and Genetics at the Democritus University of Thrace, “The phenomenon we observed in Aitoliko is not unprecedented. It is a seasonal phenomenon that occurs mainly at the end of the summer and early autumn, and is caused by the spiders of the genus Tetragnatha.”

Apparently, unusually warm weather is to blame ― or credit, depending on how you look at it ― for the phenomenon. Warm temperatures lead to an uptick in mosquitoes and gnats, i.e., delicious spider food.

“It’s caused by an overpopulation of spiders … there is an abundance of food available,” biologist Euterpe Patetsini told Greek media outlet Alpha TV.

Trending Blogs

Recently Viewed Blogs

Relax its just life