Adenosine diphosphate

Adenosine diphosphate known as adenosine pyrophosphate, is an important organic compound in metabolism and is essential to the flow of energy in living cells. ADP consists of three important structural components: a sugar backbone attached to adenine and two phosphate groups bonded to the 5 carbon atom of ribose; the diphosphate group of ADP is attached to the 5’ carbon of the sugar backbone, while the adenosine attaches to the 1’ carbon. ADP can be interconverted to adenosine adenosine monophosphate. ATP contains one more phosphate group than does ADP. AMP contains one fewer phosphate group. Energy transfer used by all living things is a result of dephosphorylation of ATP by enzymes known as ATPases; the cleavage of a phosphate group from ATP results in the coupling of energy to metabolic reactions and a by-product of ADP. ATP is continually reformed from lower-energy species ADP and AMP; the biosynthesis of ATP is achieved throughout processes such as substrate-level phosphorylation, oxidative phosphorylation, photophosphorylation, all of which facilitate the addition of a phosphate group to ADP.

ADP cycling supplies the energy needed to do work in a biological system, the thermodynamic process of transferring energy from one source to another. There are two types of energy: kinetic energy. Potential energy can be thought of as stored energy, or usable energy, available to do work. Kinetic energy is the energy of an object as a result of its motion; the significance of ATP is in its ability to store potential energy within the phosphate bonds. The energy stored between these bonds can be transferred to do work. For example, the transfer of energy from ATP to the protein myosin causes a conformational change when connecting to actin during muscle contraction, it takes multiple reactions between myosin and actin to produce one muscle contraction, therefore, the availability of large amounts of ATP is required to produce each muscle contraction. For this reason, biological processes have evolved to produce efficient ways to replenish the potential energy of ATP from ADP. Breaking one of ATP's phosphorus bonds generates 30.5 kilojoules per Mole of ATP.

ADP can be converted, or powered back to ATP through the process of releasing the chemical energy available in food. Plants use photosynthetic pathways to convert and store energy from sunlight conversion of ADP to ATP. Animals use the energy released in the breakdown of glucose and other molecules to convert ADP to ATP, which can be used to fuel necessary growth and cell maintenance; the ten-step catabolic pathway of glycolysis is the initial phase of free-energy release in the breakdown of glucose and can be split into two phases, the preparatory phase and payoff phase. ADP and phosphate are needed as precursors to synthesize ATP in the payoff reactions of the TCA cycle and oxidative phosphorylation mechanism. During the payoff phase of glycolysis, the enzymes phosphoglycerate kinase and pyruvate kinase facilitate the addition of a phosphate group to ADP by way of substrate-level phosphorylation. Glycolysis consists of 10 steps; the net reaction for the overall process of glycolysis is: Glucose + 2 NAD+ + 2 Pi + 2 ADP → 2 pyruvate + 2 ATP + 2 NADH + 2 H2OSteps 1 and 3 require the input of energy derived from the hydrolysis of ATP to ADP and Pi, whereas steps 7 and 10 require the input of ADP, each yielding ATP.

The enzymes necessary to break down glucose are found in the cytoplasm, the viscous fluid that fills living cells, where the glycolytic reactions take place. The citric acid cycle known as the Krebs cycle or the TCA cycle is an 8-step process that takes the pyruvate generated by glycolysis and generates 4 NADH, FADH2, GTP, further converted to ATP, it is only in step 5, where GTP is generated, by succinyl-CoA synthetase, converted to ATP, that ADP is used. Oxidative phosphorylation produces 26 of the 30 equivalents of ATP generated in cellular respiration by transferring electrons from NADH or FADH2 to O2 through electron carriers; the energy released when electrons are passed from higher-energy NADH or FADH2 to the lower-energy O2 is required to phosphorylate ADP and once again generate ATP. It is this energy coupling and phosphorylation of ADP to ATP that gives the electron transport chain the name oxidative phosphorylation. During the initial phases of glycolysis and the TCA cycle, cofactors such as NAD+ donate and accept electrons that aid in the electron transport chain's ability to produce a proton gradient across the inner mitochondrial membrane.

The ATP synthase complex exists within protrudes into the matrix. The energy derived as a result of the chemical gradient is used to synthesize ATP by coupling the reaction of inorganic phosphate to ADP in the active site of the ATP synthase enzyme. Under normal conditions, small disk-shape platelets circulate in the blood and without interaction with one another. ADP is released upon platelet activation. ADP interacts with a family of ADP receptors found on platelets. P2Y1 receptors initiate platelet aggregation and shape change as a result of interactions with ADP. P2Y12 receptors further draw forth the completion of aggregation. ADP in the blood is converted to adenosine by the action of ecto-ADPases, inhibiting further platelet activation via adenosine receptors

List of EastEnders characters (2015)

The following is a list of characters that first appeared in the BBC soap opera EastEnders in 2015, by order of first appearance. All characters were introduced by the show's executive producer Dominic Treadwell-Collins. January saw the arrival of the year's first baby, Matthew Mitchell Cotton, son of Ronnie Mitchell and Charlie Cotton; the following month saw the show celebrate its 30th anniversary with a live week, which oversaw the live arrivals of Vincent Hubbard, the second baby born in 2015, Pearl Fox-Hubbard, Vincent's daughter with Kim Fox-Hubbard. In March, Claudette Hubbard arrived as Donna Yates' foster mother and an acquaintance of Les Coker followed by Stan Carter's friend Cyril Bishop and Sharon Mitchell's aunt Margaret Midhurst, whilst Denise van Outen joined in April as Karin Smart. May saw the arrivals of June Whitfield as Sister Ruth and Linda Carter's son Ollie Carter, the year's third baby, Mo Harris' business associate Fat Elvis and Kush Kazemi's mother, Carmel. Paul Coker, the grandson of Les and Pam Coker, was introduced in June, as was Jade Green, the long-lost daughter of Shabnam Masood and Dean Wicks.

After Kathy Sullivan's surprise return during the 30th anniversary in February, her husband Gavin Sullivan made his debut in August. September saw the arrivals of Max Branning's prosecution lawyer Hazel Warren and Louie Beale, the baby son of Lauren Branning and Peter Beale. In October, Elaine Peacock's toyboy lover Jason Adams was introduced, as well as first transgender character to be played by a transgender actor, Kyle Slater. December saw the birth of the year's fifth baby and Stacey Slater's son, Arthur Fowler. Matthew Mitchell Cotton, portrayed by Zack Karbritz, is the son of Charlie Cotton and Ronnie Mitchell, he is born during the episode broadcast on 1 January 2015 on his parents' wedding day. Matthew is born, she is placed in a coma, due to her injuries. Her sister, Roxy Mitchell and her boyfriend Aleks Shirovs look after Matthew when Charlie refuses to see him, due to Ronnie's absence. Charlie's father, Nick Cotton, takes Matthew from Roxy, attempting to force Charlie to see his son but Charlie refuses and gives him back to Roxy.

Aleks suggests naming him Matthew after Nick's mother Dot Branning quotes from the Gospel of Matthew. Aleks's daughter Ineta Shirovs becomes fed up with Aleks looking after Matthew and takes him to the bus stop, so they can go to the hospital. Charlie takes Matthew home, he and Roxy share residency until Ronnie is discharged from hospital. When Matthew is nine months old, he stays with Ronnie when she and Charlie separate, although Charlie vows to fight for custody; when Charlie tells Roxy he wants to take Matthew to France, she tells Ronnie. Roxy goes with Charlie but he soon realises that Ronnie and Roxy are working together when he sees Roxy looking at her phone and Fatboy tells him that Vincent has told Ronnie, so he decides to leave with Matthew alone. However, Ronnie arrives before Charlie can board his train, convinces him not to make the same mistakes as Nick did. Charlie leaves Matthew with Ronnie. Four days Charlie returns to Walford, having been persuaded by Dot to fight for custody, but Ronnie turns nasty when Charlie threatens to tell the police that she murdered Carl White and says that she will never see Matthew again.

She and former boyfriend, Vincent Hubbard, confront Charlie. Matthew lives with Ronnie and her ex-husband, Jack Branning, when they reunite in March 2016 and Jack and Roxy's daughter, Amy Mitchell moves in. Matthew is nearly hit by a car when Hannah Reynolds steps into the road whilst holding him, but is saved by Andy Flynn, who pushes them out of the way of the approaching car. On the night that Ronnie and Jack remarry on New Year's Day 2017, Ronnie and Roxy die, leaving Matthew in Jack and Glenda Mitchell's care when she moves in to help bring up the children. Glenda, Amy and Jack's son Ricky Mitchell grow close but she realises she is not what Jack, Amy and Matthew need to get through Ronnie and Roxy's deaths so decides to leave Walford, while promising to remain a part of Amy and Matthew's lives. After taking Matthew to the garden centre in February 2017, Dot has an accident in her car due to her eye sight, she and Matthew are unharmed and taken home by the police. When Matthew goes missing, Jack's brother, Max Branning, tells Jack that Matthew is at Dot's and when Jack goes to get him, Charlie answers the door, telling Jack they need to talk about Matthew.

Jack reluctantly lets Charlie look after Charlie. Charlie tells Dot that he has seen a solicitor about Matthew, who he plans to take back to Ireland with him. Dot tells Jack that Charlie is going to take Matthew back to Ireland and Charlie and Jack argue about it, with Jack telling Charlie that he swore on Ronnie's grave to never leave Amy and Matthew; when Charlie provokes Jack by saying Ronnie deserved to die, Jack punches him and Max tells Jack he may have lost his chances of keeping Matthew. Max learns that Jack still may get to keep Matthew despite the fight with Jack, so Max visits Charlie and beats him up to make it look like Jack did it. In April 2017, Jack is charged with assault. Dot attempts to mediate between Charlie and Jack, but they fail to come up with any solution and Jack plans to go on the run with Amy and Matthew, but Dot tells Max and they talk him out of it. Charlie watches Honey Mitchell in the park with Amy, Ricky and her c


C22orf23 is a protein which in humans is encoded by the C22orf23 gene. Its predicted secondary structure consists of disordered/coil regions, it is expressed in many tissues and highest in the testes and it is conserved across many orthologs. C22orf23 is a gene found in homo sapiens, it is located on Chromosome 22 on the minus strand, map position 22q13.1. It spans 10,620 base pairs, its mRNA transcript has 7 exons. Its predicted function is protein binding, molecular function. C22orf23's aliases are: UPF0193 Protein EVG1, DJ1039K5.6, EVG1 FLJ32787, LOC84645. The protein encoded by the mRNA sequence is 217 amino acids in length and has a predicted molecular mass of 25 kDa; the predicted isoelectric point is 9.8. It is located in the nucleus, it is predicted to be an intracellular protein and does not have any predicted transmembrane domains. Due to its location and lack of predicted transmembrane domains, the protein structure is a globular protein. C22orf23 has many predicted post-translational modifications such as: phosphorylation sites, cell attachment sequences, N-myristoylation sites, O-linked glycosylation sites, glycation sites, Ac-ASQK cleaved-acetylated sites, Sumoylation sites.

Many of the predicted phosphorylation sites were predicted to be O-linked glycosylation sites thus the phosphorylation site could be blocked altering that domain's structure or function. The predicted secondary structure consists of disordered/coil regions; the predicted secondary structure model has a 28% coverage of the amino acid sequence with a 42.9% confidence. There are no known paralogs to C22orf23. Orthologs can be found in most major groups of species ranging from most similar in primates to most distant in a member of phylum Chytridiomycota; this includes: mammals, birds, bony fish, cartilaginous fish and fungi. Orthologs may have first appeared in fungi however it is uncertain; this table lists several orthologs for C22orf23 and includes their species name, common name, taxonomic order, accession number, sequence length, sequence similarity, evolutionary date of divergence. The core promoter is GXP_7541220, its coordinates are 37953445-37954669 and it is 1225 base pairs long. Protein expression is highest in the testes however it is expressed at low levels in many other tissues such as: brain, stomach, thyroid, urinary bladder, endometrium and appendix, bone marrow, adipose and ovary.

Expression in orthologs Rattus norvegicus, is expressed in the testes with low levels of expression in the: kidneys, lungs and uterus. Mus musculus is expressed in the adrenal and testes, notably expressed in the: bladder, heart, lungs and mammary gland. There are several predicted protein interactions: Cyclin-D1-binding protein 1 which may regulate cell cycle progression, Vacuolar protein sorting-associated protein 28 homolog, involved as a regulator of vesicular trafficking, UPF0739 protein C1orf74, estrogen related receptor gamma; these interacting proteins were identified as either having direct interactions or physical associations. They were identified through a variety of detection methods including affinity chromatography, 2 hybrid prey pooling, 2 hybrid array, it has predicted protein interactions with SH3 domain containing 19, EvC ciliary complex subunit 1, RIMS binding protein 3B, RIMS binding protein 3C,TSSK6-activating co-chaperone protein, V-set and immunoglobulin domain containing 8, family with sequence similarity 124 member B, small nucleolar RNA host gene 28, transmembrane protein 200B.

Evidence suggesting a functional link for these interactions were supported through Co-mention on PubMed. C22orf23 was identified as belonging to one of two groups of pooled serum samples in a study that analyzed the difference between serum glycoproteins of hepatocellular carcinoma and that of normal serum. Deletions of parts of C22orf23 and several other genes including SOX10 has been observed in patients with peripheral demyelinating neuropathy, central demyelinating leukodystrophy, Waardenburg Syndrome, Hirschsprung disease and is therefore, suggested to be a potential factor involved in these ailments. C22orf23 was mentioned in a study of mutation profiles from ER+ breast cancer samples taken from postmenopausal patience. There were mutations found. In a study of epigenetic alterations involved in coronary artery disease, C22orf23 was found to have altered epigenetic modifications which could be involved in novel genes in Coronary artery disease. In a study that attempts to predict imprinted genes that maybe linked to Human disorders, C22orf23 was identified as homologous of imprinted Gene candidates showing linkage to schizophrenia.

In another study it was listed as being a potently regulated protein in uterine leiomyoma. There are a total of 3340 SNPs within the 5’ and 3’ UTR, exons, as well as some genes near the 5’ and 3’ UTR. There is a total of 225 SNPs within the coding sequence; some of the SNPs occur in conserved amino acids within the coding sequence and some reported have one or more types of validation. Some of the SNPs have high heterozygosity scores and thus have a presence in the population