Alternative splicing, or differential splicing, is a regulated process during gene expression that results in a single gene coding for multiple proteins. In this process, particular exons of a gene may be included within or excluded from the final, processed messenger RNA produced from that gene; the proteins translated from alternatively spliced mRNAs will contain differences in their amino acid sequence and in their biological functions. Notably, alternative splicing allows the human genome to direct the synthesis of many more proteins than would be expected from its 20,000 protein-coding genes. Alternative splicing occurs as a normal phenomenon in eukaryotes, where it increases the biodiversity of proteins that can be encoded by the genome. There are numerous modes of alternative splicing observed, of which the most common is exon skipping. In this mode, a particular exon may be included in mRNAs under some conditions or in particular tissues, omitted from the mRNA in others; the production of alternatively spliced mRNAs is regulated by a system of trans-acting proteins that bind to cis-acting sites on the primary transcript itself.
Such proteins include splicing activators that promote the usage of a particular splice site, splicing repressors that reduce the usage of a particular site. Mechanisms of alternative splicing are variable, new examples are being found through the use of high-throughput techniques. Researchers hope to elucidate the regulatory systems involved in splicing, so that alternative splicing products from a given gene under particular conditions could be predicted by a "splicing code". Abnormal variations in splicing are implicated in disease. Abnormal splicing variants are thought to contribute to the development of cancer, splicing factor genes are mutated in different types of cancer. Alternative splicing was first observed in 1977; the Adenovirus produces five primary transcripts early in its infectious cycle, prior to viral DNA replication, an additional one after DNA replication begins. The early primary transcripts continue to be produced; the additional primary transcript produced late in infection is large and comes from 5/6 of the 32kb adenovirus genome.
This is much larger. Researchers found that the primary RNA transcript produced by adenovirus type 2 in the late phase was spliced in many different ways, resulting in mRNAs encoding different viral proteins. In addition, the primary transcript contained multiple polyadenylation sites, giving different 3’ ends for the processed mRNAs. In 1981, the first example of alternative splicing in a transcript from a normal, endogenous gene was characterized; the gene encoding the thyroid hormone calcitonin was found to be alternatively spliced in mammalian cells. The primary transcript from this gene contains 6 exons. Another mRNA is produced from this pre-mRNA by skipping exon 4, includes exons 1–3, 5, 6, it encodes a protein known as CGRP. Examples of alternative splicing in immunoglobin gene transcripts in mammals were observed in the early 1980s. Since alternative splicing has been found to be ubiquitous in eukaryotes; the "record-holder" for alternative splicing is a D. melanogaster gene called Dscam, which could have 38,016 splice variants.
Five basic modes of alternative splicing are recognized. Exon skipping or cassette exon: in this case, an exon may be spliced out of the primary transcript or retained; this is the most common mode in mammalian pre-mRNAs. Mutually exclusive exons: One of two exons is retained in mRNAs after splicing, but not both. Alternative donor site: An alternative 5' splice junction is used, changing the 3' boundary of the upstream exon. Alternative acceptor site: An alternative 3' splice junction is used, changing the 5' boundary of the downstream exon. Intron retention: A sequence may be spliced out as an intron or retained; this is distinguished from exon skipping. If the retained intron is in the coding region, the intron must encode amino acids in frame with the neighboring exons, or a stop codon or a shift in the reading frame will cause the protein to be non-functional; this is the rarest mode in mammals. In addition to these primary modes of alternative splicing, there are two other main mechanisms by which different mRNAs may be generated from the same gene.
Use of multiple promoters is properly described as a transcriptional regulation mechanism rather than alternative splicing. At the other end, multiple polyadenylation sites provide different 3' end points for the transcript. Both of these mechanisms are found in combination with alternative splicing and provide additional variety in mRNAs derived from a gene; these modes describe basic splicing mechanisms, but may be inadequate to describe complex splicing events. For instance, the figure to the right shows 3 spliceforms from the mouse hyaluronidase 3 gene. Comparing the exonic structure shown in the first line with the one in the second line shows intron retention, whereas the comparison between the second and the third spliceform exhibits exon skipping. A model nomenclature to un
Developmental biology is the study of the process by which animals and plants grow and develop. Developmental biology encompasses the biology of regeneration, asexual reproduction and the growth and differentiation of stem cells in the adult organism. In the late 20th century, the discipline transformed into evolutionary developmental biology; the main processes involved in the embryonic development of animals are: regional specification, cell differentiation and the overall control of timing explored in evolutionary developmental biology: Regional specification refers to the processes that create spatial pattern in a ball or sheet of similar cells. This involves the action of cytoplasmic determinants, located within parts of the fertilized egg, of inductive signals emitted from signaling centers in the embryo; the early stages of regional specification do not generate functional differentiated cells, but cell populations committed to develop to a specific region or part of the organism. These are defined by the expression of specific combinations of transcription factors.
Morphogenesis relates to the formation of three-dimensional shape. It involves the orchestrated movements of cell sheets and of individual cells. Morphogenesis is important for creating the three germ layers of the early embryo and for building up complex structures during organ development. Cell differentiation relates to the formation of functional cell types such as nerve, secretory epithelia etc. Differentiated cells contain large amounts of specific proteins associated with the cell function. Growth involves both an overall increase in size, the differential growth of parts which contributes to morphogenesis. Growth occurs through cell division but through changes of cell size and the deposition of extracellular materials; the control of timing of events and the integration of the various processes with one another is the least well understood area of the subject. It remains unclear; the development of plants involves similar processes to that of animals. However plant cells are immotile so morphogenesis is achieved by differential growth, without cell movements.
The inductive signals and the genes involved are different from those that control animal development. Cell differentiation is the process. For example, muscle fibers and hepatocytes are well known types of differentiated cell. Differentiated cells produce large amounts of a few proteins that are required for their specific function and this gives them the characteristic appearance that enables them to be recognized under the light microscope; the genes encoding these proteins are active. Their chromatin structure is open, allowing access for the transcription enzymes, specific transcription factors bind to regulatory sequences in the DNA in order to activate gene expression. For example, NeuroD is a key transcription factor for neuronal differentiation, myogenin for muscle differentiation, HNF4 for hepatocyte differentiation. Cell differentiation is the final stage of development, preceded by several states of commitment which are not visibly differentiated. A single tissue, formed from a single type of progenitor cell or stem cell consists of several differentiated cell types.
Control of their formation involves a process of lateral inhibition, based on the properties of the Notch signaling pathway. For example, in the neural plate of the embryo this system operates to generate a population of neuronal precursor cells in which NeuroD is expressed. Regeneration indicates the ability to regrow a missing part; this is prevalent amongst plants, which show continuous growth, among colonial animals such as hydroids and ascidians. But most interest by developmental biologists has been shown in the regeneration of parts in free living animals. In particular four models have been the subject of much investigation. Two of these have the ability to regenerate whole bodies: Hydra, which can regenerate any part of the polyp from a small fragment, planarian worms, which can regenerate both heads and tails. Both of these examples have continuous cell turnover fed by stem cells and, at least in planaria, at least some of the stem cells have been shown to be pluripotent; the other two models show only distal regeneration of appendages.
These are the insect appendages the legs of hemimetabolous insects such as the cricket, the limbs of urodele amphibians. Considerable information is now available about amphibian limb regeneration and it is known that each cell type regenerates itself, except for connective tissues where there is considerable interconversion between cartilage and tendons. In terms of the pattern of structures, this is controlled by a re-activation of signals active in the embryo. There is still debate about the old question of whether regeneration is a "pristine" or an "adaptive" property. If the former is the case, with improved knowledge, we might expect to be able to improve regenerative ability in humans. If the latter each instance of regeneration is presumed to have arisen by natural selection in circumstances particular to the species, so no general rules would be expected; the sperm and egg fuse in the process of fertilization to form a fertilized egg, or zygote. This undergoes a period of divisions to form a ball or sheet of similar cells called a blastula or blastoderm.
These cell divisions are rapid with no growth so the daughter cells are half the size of the mother cell and the whole embryo stays ab
In biology, a gene is a sequence of nucleotides in DNA or RNA that codes for a molecule that has a function. During gene expression, the DNA is first copied into RNA; the RNA can be directly functional or be the intermediate template for a protein that performs a function. The transmission of genes to an organism's offspring is the basis of the inheritance of phenotypic trait; these genes make up different DNA sequences called genotypes. Genotypes along with developmental factors determine what the phenotypes will be. Most biological traits are under the influence of polygenes as well as gene–environment interactions; some genetic traits are visible, such as eye color or number of limbs, some are not, such as blood type, risk for specific diseases, or the thousands of basic biochemical processes that constitute life. Genes can acquire mutations in their sequence, leading to different variants, known as alleles, in the population; these alleles encode different versions of a protein, which cause different phenotypical traits.
Usage of the term "having a gene" refers to containing a different allele of the same, shared gene. Genes evolve due to natural selection / survival of the fittest and genetic drift of the alleles; the concept of a gene continues to be refined. For example, regulatory regions of a gene can be far removed from its coding regions, coding regions can be split into several exons; some viruses store their genome in RNA instead of DNA and some gene products are functional non-coding RNAs. Therefore, a broad, modern working definition of a gene is any discrete locus of heritable, genomic sequence which affect an organism's traits by being expressed as a functional product or by regulation of gene expression; the term gene was introduced by Danish botanist, plant physiologist and geneticist Wilhelm Johannsen in 1909. It is inspired by the ancient Greek: γόνος, that means offspring and procreation; the existence of discrete inheritable units was first suggested by Gregor Mendel. From 1857 to 1864, in Brno, he studied inheritance patterns in 8000 common edible pea plants, tracking distinct traits from parent to offspring.
He described these mathematically as 2n combinations where n is the number of differing characteristics in the original peas. Although he did not use the term gene, he explained his results in terms of discrete inherited units that give rise to observable physical characteristics; this description prefigured Wilhelm Johannsen's distinction between phenotype. Mendel was the first to demonstrate independent assortment, the distinction between dominant and recessive traits, the distinction between a heterozygote and homozygote, the phenomenon of discontinuous inheritance. Prior to Mendel's work, the dominant theory of heredity was one of blending inheritance, which suggested that each parent contributed fluids to the fertilisation process and that the traits of the parents blended and mixed to produce the offspring. Charles Darwin developed a theory of inheritance he termed pangenesis, from Greek pan and genesis / genos. Darwin used the term gemmule to describe hypothetical particles. Mendel's work went unnoticed after its first publication in 1866, but was rediscovered in the late 19th century by Hugo de Vries, Carl Correns, Erich von Tschermak, who reached similar conclusions in their own research.
In 1889, Hugo de Vries published his book Intracellular Pangenesis, in which he postulated that different characters have individual hereditary carriers and that inheritance of specific traits in organisms comes in particles. De Vries called these units "pangenes", after Darwin's 1868 pangenesis theory. Sixteen years in 1905, Wilhelm Johannsen introduced the term'gene' and William Bateson that of'genetics' while Eduard Strasburger, amongst others, still used the term'pangene' for the fundamental physical and functional unit of heredity. Advances in understanding genes and inheritance continued throughout the 20th century. Deoxyribonucleic acid was shown to be the molecular repository of genetic information by experiments in the 1940s to 1950s; the structure of DNA was studied by Rosalind Franklin and Maurice Wilkins using X-ray crystallography, which led James D. Watson and Francis Crick to publish a model of the double-stranded DNA molecule whose paired nucleotide bases indicated a compelling hypothesis for the mechanism of genetic replication.
In the early 1950s the prevailing view was that the genes in a chromosome acted like discrete entities, indivisible by recombination and arranged like beads on a string. The experiments of Benzer using mutants defective in the rII region of bacteriophage T4 showed that individual genes have a simple linear structure and are to be equivalent to a linear section of DNA. Collectively, this body of research established the central dogma of molecular biology, which states that proteins are translated from RNA, transcribed from DNA; this dogma has since been shown to have exceptions, such as reverse transcription in retroviruses. The modern study of genetics at the level of DNA is known as molecular genetics. In 1972, Walter Fiers and his team were the first to determine the sequence of a gene: that of Bacteriophage MS2 coat protein; the subsequent development of chain-termination DNA sequencing in 1977 by Frederick Sanger improved the efficiency of sequencing and turned it into a routine laboratory tool.
An automated version of the Sanger method was used in early phases of the
Pharmacology is the branch of biology concerned with the study of drug action, where a drug can be broadly defined as any man-made, natural, or endogenous molecule which exerts a biochemical or physiological effect on the cell, organ, or organism. More it is the study of the interactions that occur between a living organism and chemicals that affect normal or abnormal biochemical function. If substances have medicinal properties, they are considered pharmaceuticals; the field encompasses drug composition and properties and drug design and cellular mechanisms, organ/systems mechanisms, signal transduction/cellular communication, molecular diagnostics, toxicology, chemical biology and medical applications and antipathogenic capabilities. The two main areas of pharmacology are pharmacokinetics. Pharmacodynamics studies the effects of a drug on biological systems, Pharmacokinetics studies the effects of biological systems on a drug. In broad terms, pharmacodynamics discusses the chemicals with biological receptors, pharmacokinetics discusses the absorption, distribution and excretion of chemicals from the biological systems.
Pharmacology is not synonymous with pharmacy and the two terms are confused. Pharmacology, a biomedical science, deals with the research and characterization of chemicals which show biological effects and the elucidation of cellular and organismal function in relation to these chemicals. In contrast, pharmacy, a health services profession, is concerned with application of the principles learned from pharmacology in its clinical settings. In either field, the primary contrast between the two are their distinctions between direct-patient care, for pharmacy practice, the science-oriented research field, driven by pharmacology; the origins of clinical pharmacology date back to the Middle Ages in Avicenna's The Canon of Medicine, Peter of Spain's Commentary on Isaac, John of St Amand's Commentary on the Antedotary of Nicholas. Clinical pharmacology owes much of its foundation to the work of William Withering. Pharmacology as a scientific discipline did not further advance until the mid-19th century amid the great biomedical resurgence of that period.
Before the second half of the nineteenth century, the remarkable potency and specificity of the actions of drugs such as morphine and digitalis were explained vaguely and with reference to extraordinary chemical powers and affinities to certain organs or tissues. The first pharmacology department was set up by Rudolf Buchheim in 1847, in recognition of the need to understand how therapeutic drugs and poisons produced their effects. Early pharmacologists focused on natural substances plant extracts. Pharmacology developed in the 19th century as a biomedical science that applied the principles of scientific experimentation to therapeutic contexts. Today pharmacologists use genetics, molecular biology and other advanced tools to transform information about molecular mechanisms and targets into therapies directed against disease, defects or pathogens, create methods for preventative care and personalized medicine; the word "pharmacology" is derived from Greek φάρμακον, pharmakon, "drug, spell" and -λογία, -logia "study of", "knowledge of".
The discipline of pharmacology can be divided into many sub disciplines each with a specific focus. Clinical pharmacology is the basic science of pharmacology with an added focus on the application of pharmacological principles and methods in the medical clinic and towards patient care and outcomes. Neuropharmacology is the study of the effects of medication on central and peripheral nervous system functioning. Psychopharmacology known as behavioral pharmacology, is the study of the effects of medication on the psyche, observing changed behaviors of the body and mind, how molecular events are manifest in a measurable behavioral form. Psychopharmacology is an interdisciplinary field which studies behavioral effects of psychoactive drugs, it incorporates approaches and techniques from neuropharmacology, animal behavior and behavioral neuroscience, is interested in the behavioral and neurobiological mechanisms of action of psychoactive drugs. Another goal of behavioral pharmacology is to develop animal behavioral models to screen chemical compounds with therapeutic potentials.
People in this field use small animals to study psychotherapeutic drugs such as antipsychotics and anxiolytics, drugs of abuse such as nicotine and methamphetamine. Ethopharmacology is a term, in use since the 1960s and derives from the Greek word ἦθος ethos meaning character and "pharmacology" the study of drug actions and mechanism. Cardiovascular pharmacology is the study of the effects of drugs on the entire cardiovascular system, including the heart and blood vessels. Pharmacogenetics is clinical testing of genetic variation that gives rise to differing response to drugs. Pharmacogenomics is the application of genomic technologies to drug discovery and further characterization of older drugs. Pharmacoepidemiology is the study of the effects of drugs in large numbers of people. Safety pharmacology specialises in detecting and investigating potential undesirable pharmacodynamic effects of new chemical entities on physiological functions in relation to exposure in the therapeutic range and above.
Systems pharmacology is
Carcinogenesis called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells. The process is characterized by changes at the cellular and epigenetic levels and abnormal cell division. Cell division is a physiological process that occurs in all tissues and under a variety of circumstances; the balance between proliferation and programmed cell death, in the form of apoptosis, is maintained to ensure the integrity of tissues and organs. According to the prevailing accepted theory of carcinogenesis, the somatic mutation theory, mutations in DNA and epimutations that lead to cancer disrupt these orderly processes by disrupting the programming regulating the processes, upsetting the normal balance between proliferation and cell death; this results in uncontrolled cell division and the evolution of those cells by natural selection in the body. Only certain mutations lead to cancer. Variants of inherited genes may predispose individuals to cancer.
In addition, environmental factors such as carcinogens and radiation cause mutations that may contribute to the development of cancer. Random mistakes in normal DNA replication may result in cancer causing mutations. A series of several mutations to certain classes of genes is required before a normal cell will transform into a cancer cell. On average, for example, 15 "driver mutations" and 60 "passenger" mutations are found in colon cancers. Mutations in genes that regulate cell division, DNA repair may result in uncontrolled cell proliferation and cancer. Cancer is fundamentally a disease of regulation of tissue growth. In order for a normal cell to transform into a cancer cell, genes that regulate cell growth and differentiation must be altered. Genetic and epigenetic changes can occur at many levels, from gain or loss of entire chromosomes, to a mutation affecting a single DNA nucleotide, or to silencing or activating a microRNA that controls expression of 100 to 500 genes. There are two broad categories of genes.
Oncogenes may be normal genes that are expressed at inappropriately high levels, or altered genes that have novel properties. In either case, expression of these genes promotes the malignant phenotype of cancer cells. Tumor suppressor genes are genes that inhibit cell division, survival, or other properties of cancer cells. Tumor suppressor genes are disabled by cancer-promoting genetic changes. Oncovirinae, viruses that contain an oncogene, are categorized as oncogenic because they trigger the growth of tumorous tissues in the host; this process is referred to as viral transformation. There is a diverse classification scheme for the various genomic changes that may contribute to the generation of cancer cells. Many of these changes are mutations, or changes in the nucleotide sequence of genomic DNA. There are many epigenetic changes that alter whether genes are expressed or not expressed. Aneuploidy, the presence of an abnormal number of chromosomes, is one genomic change, not a mutation, may involve either gain or loss of one or more chromosomes through errors in mitosis.
Large-scale mutations involve the gain of a portion of a chromosome. Genomic amplification occurs when a cell gains many copies of a small chromosomal region containing one or more oncogenes and adjacent genetic material. Translocation occurs when two separate chromosomal regions become abnormally fused at a characteristic location. A well-known example of this is the Philadelphia chromosome, or translocation of chromosomes 9 and 22, which occurs in chronic myelogenous leukemia, results in production of the BCR-abl fusion protein, an oncogenic tyrosine kinase. Small-scale mutations include point mutations and insertions, which may occur in the promoter of a gene and affect its expression, or may occur in the gene's coding sequence and alter the function or stability of its protein product. Disruption of a single gene may result from integration of genomic material from a DNA virus or retrovirus, such an event may result in the expression of viral oncogenes in the affected cell and its descendants.
DNA damage is considered to be the primary cause of cancer. More than 60,000 new occurring DNA damages arise, on average, per human cell, per day, due to endogenous cellular processes. Additional DNA damages can arise from exposure to exogenous agents; as one example of an exogenous carcinogeneic agent, tobacco smoke causes increased DNA damage, these DNA damages cause the increase of lung cancer due to smoking. In other examples, UV light from solar radiation causes DNA damage, important in melanoma, helicobacter pylori infection produces high levels of reactive oxygen species that damage DNA and contributes to gastric cancer, the Aspergillus metabolite, aflatoxin, is a DNA damaging agent, causative in liver cancer. DNA damages can be caused by endogenous agents. Macrophages and neutrophils in an inflamed colonic epithelium are the source of reactive oxygen species causing the DNA damages that initiate colonic tumorigenesis, bile acids, at high levels in the colons of humans eating a high fat diet cause DNA damage and contribute to colon cancer.
Such exogenous and endogenous sources of DNA damage are indicated in the boxes at the top of the figure in this section. The central role of DNA damage in progression to cancer is indicated at the second level of the figure; the central elements of DNA damage, epigenetic alterations and deficient DNA repair in progression to cancer are shown in red. A deficiency in DNA repair would cause more
Chromosome 3 is one of the 23 pairs of chromosomes in humans. People have two copies of this chromosome. Chromosome 3 spans 200 million base pairs and represents about 6.5 percent of the total DNA in cells. The following are some of the gene count estimates of human chromosome 3; because researchers use different approaches to genome annotation their predictions of the number of genes on each chromosome varies. Among various projects, the collaborative consensus coding sequence project takes an conservative strategy. So CCDS's gene number prediction represents a lower bound on the total number of human protein-coding genes; the following is a partial list of genes on human chromosome 3. For complete list, see the link in the infobox on the right. Partial list of the genes located on p-arm of human chromosome 3: Partial list of the genes located on q-arm of human chromosome 3: The following diseases and disorders are some of those related to genes on chromosome 3: National Institutes of Health. "Chromosome 3".
Genetics Home Reference. Retrieved 2017-05-06. "Chromosome 3". Human Genome Project Information Archive 1990–2003. Retrieved 2017-05-06
Amino acids are organic compounds containing amine and carboxyl functional groups, along with a side chain specific to each amino acid. The key elements of an amino acid are carbon, hydrogen and nitrogen, although other elements are found in the side chains of certain amino acids. About 500 occurring amino acids are known and can be classified in many ways, they can be classified according to the core structural functional groups' locations as alpha-, beta-, gamma- or delta- amino acids. In the form of proteins, amino acid residues form the second-largest component of human muscles and other tissues. Beyond their role as residues in proteins, amino acids participate in a number of processes such as neurotransmitter transport and biosynthesis. In biochemistry, amino acids having both the amine and the carboxylic acid groups attached to the first carbon atom have particular importance, they are known as α-amino acids. They include the 22 proteinogenic amino acids, which combine into peptide chains to form the building-blocks of a vast array of proteins.
These are all L-stereoisomers, although a few D-amino acids occur in bacterial envelopes, as a neuromodulator, in some antibiotics. Twenty of the proteinogenic amino acids are encoded directly by triplet codons in the genetic code and are known as "standard" amino acids; the other two are selenocysteine, pyrrolysine. Pyrrolysine and selenocysteine are encoded via variant codons. N-formylmethionine is considered as a form of methionine rather than as a separate proteinogenic amino acid. Codon–tRNA combinations not found in nature can be used to "expand" the genetic code and form novel proteins known as alloproteins incorporating non-proteinogenic amino acids. Many important proteinogenic and non-proteinogenic amino acids have biological functions. For example, in the human brain and gamma-amino-butyric acid are the main excitatory and inhibitory neurotransmitters. Hydroxyproline, a major component of the connective tissue collagen, is synthesised from proline. Glycine is a biosynthetic precursor to porphyrins used in red blood cells.
Carnitine is used in lipid transport. Nine proteinogenic amino acids are called "essential" for humans because they cannot be produced from other compounds by the human body and so must be taken in as food. Others may be conditionally essential for medical conditions. Essential amino acids may differ between species; because of their biological significance, amino acids are important in nutrition and are used in nutritional supplements, fertilizers and food technology. Industrial uses include the production of drugs, biodegradable plastics, chiral catalysts; the first few amino acids were discovered in the early 19th century. In 1806, French chemists Louis-Nicolas Vauquelin and Pierre Jean Robiquet isolated a compound in asparagus, subsequently named asparagine, the first amino acid to be discovered. Cystine was discovered in 1810, although its monomer, remained undiscovered until 1884. Glycine and leucine were discovered in 1820; the last of the 20 common amino acids to be discovered was threonine in 1935 by William Cumming Rose, who determined the essential amino acids and established the minimum daily requirements of all amino acids for optimal growth.
The unity of the chemical category was recognized by Wurtz in 1865, but he gave no particular name to it. Usage of the term "amino acid" in the English language is from 1898, while the German term, Aminosäure, was used earlier. Proteins were found to yield amino acids after enzymatic acid hydrolysis. In 1902, Emil Fischer and Franz Hofmeister independently proposed that proteins are formed from many amino acids, whereby bonds are formed between the amino group of one amino acid with the carboxyl group of another, resulting in a linear structure that Fischer termed "peptide". In the structure shown at the top of the page, R represents a side chain specific to each amino acid; the carbon atom next to the carboxyl group is called the α–carbon. Amino acids containing an amino group bonded directly to the alpha carbon are referred to as alpha amino acids; these include amino acids such as proline which contain secondary amines, which used to be referred to as "imino acids". The alpha amino acids are the most common form found in nature, but only when occurring in the L-isomer.
The alpha carbon is a chiral carbon atom, with the exception of glycine which has two indistinguishable hydrogen atoms on the alpha carbon. Therefore, all alpha amino acids but glycine can exist in either of two enantiomers, called L or D amino acids, which are mirror images of each other. While L-amino acids represent all of the amino acids found in proteins during translation in the ribosome, D-amin