The Jolson Story is a 1946 American Technicolor musical biography film which purports to tell the life story of singer Al Jolson. It stars Larry Parks as Jolson, Evelyn Keyes as Julie Benson, William Demarest as his manager, Ludwig Donath and Tamara Shayne as his parents, Scotty Beckett as the young Jolson; the Columbia Pictures production was written by Sidney Buchman, Harry Chandlee, Stephen Longstreet and Andrew Solt. The dramatic scenes were directed by Alfred E. Green, with the musical sequences directed by Joseph H. Lewis. A sequel called Jolson Sings Again was released in 1949. American burlesque performer Steve Martin offers to play a song for his audience, if they agree to sing along. Only one person does sing, a young boy named Asa Yoelson. Steve is bowled over by the boy's voice, but Asa realizes he should be singing at the synagogue with his father, Cantor Yoelson. Asa arrives late, is reprimanded by his strict father. Asa is reluctant to explain where he was, he explains that he heard Asa sing at the burlesque house, that he wants Asa to be part of his act.
Papa Yoelson refuses to consider it. Asa is determined to be in the act, runs away to Baltimore, where he is taken to a home for boys; the kindly superintendent, Father McGee, is moved by Asa's determination, finds Steve Martin, but he notifies Asa's parents. When they appear, Asa tells them that he will keep running away until they allow him to go into show business. Asa's mother believes that it would be better to give Asa what he wants than have him running away all the time. On stage, Asa gets bored with singing songs the same way all the time, begins to improvise, much to Steve Martin's annoyance; when his voice breaks in the middle of a number, he starts whistling instead, but is unhappy and wants to go home. Steve says that they can work on stage together, which Asa has always wanted - he has only stood in the audience. Asa changes his mind, his name: he begins to perform as Al Jolson. At a variety show, blackface entertainer Tom Baron passes out drunk, Al goes on in his place. Two theatrical entrepreneurs, Oscar Hammerstein and Lew Dockstader, are in the audience.
Dockstader realizes that it was Al, on stage, hires him join his minstrel show. Meanwhile, who has not seen Baron work before, offers him a job at his theatre. Jolson doesn't wish to leave Steve Martin, but Steve thinks it is a perfect opportunity for him, deliberately leads him onto the wrong train. Jolson enjoys his new job, Dokstader is impressed by his abilities, but Jolson wants to add some new songs to the repertoire, he tries to discuss it with his boss, but Dokstader fobs him off. One night, Jolson is out walking when he hears a band playing exciting jazz music. Dockstader wishes him luck for the future. Al visits his parents, but does not stay long, because he receives a call from Tom Baron, now a theater manager – his singing was so bad that Hammerstein paid him off if he agreed to quit singing for good. Baron invites Al to join his Broadway show. Al insists on choosing his own material. Tom agrees. Al sings many new songs, including his signature tune, "Mammy", he becomes so popular that he becomes the leading player and takes the show on tour.
At a Sunday night concert, Al, who has never been interested in girls, meets an up-and-coming dancer named Julie Benson. It is love at first sight for Al, only a few hours after meeting her, he proposes to her.. She is not in love with him, but he will not take no for an answer, she agrees to consider it. Julie falls in love with Al, after he supports her during her first show, they marry, but Julie is not as fond of show business. Al persuades her to continue with it, she stars in a string of pictures, becomes a success. They star in a film together, but Julie can't stand any more; when Al realises that the only way to keep Julie is to quit showbusiness, he agrees to quit, they move to the country. Al refuses all job offers and will not sing for family and friends, but one night, at a dinner celebrating the wedding anniversary of Al's parents, Papa Yoelson persuades his son to join him in a song – the music he and Mama Yoelson danced to at their wedding – and Al gets caught up in it and ends up improvising words.
Tom Baron suggests they go to a nightclub and see the early floor show. Jolson is reluctant, fearing he'll be recognized, the bandleader indeed does introduce him as he sits at the table with the others; the crowd demands a song and though he tries to fob the crowd off, it is no use and he has to sing. He agrees to sing one song, but the crowd yell for more, he ends up taking over the show. Julie realizes he is happier than he leaves while he's performing, she walks out of the picture, out of his life, leaving Al to his first love: singing. Some of the plot details were fictionalized. There is no evidence that Jolson appeared as a child singer, he was brought up by his sister, not his mother. Jolson had three managers, who were combined into the William Demarest character, "Steve Martin". Ruby Keeler refused to allow her name to be used, so the writers used an alias, "Julie Benson". Larry Parks' vocals were recorded by Al Jolson. Al Jolson, determined to appear on screen somehow, persuade
Wilbur Bernard Ware was an American jazz double bassist. He was a staff bassist at Riverside in the 1950s, recording with J. R. Monterose, Toots Thielemans, Tina Brooks, Zoot Sims, Grant Green. Ware taught himself to play bass. In the 1940s, he worked with Stuff Smith, Sonny Stitt, Roy Eldridge, he recorded with Sun Ra in the early 1950s. In the 1950s, settling in New York City, Ware played with Eddie Vinson, Art Blakey, Buddy DeFranco, his only album recorded as a leader during his lifetime was The Chicago Sound, from 1957 when he worked for Riverside. He made jazz instructional albums for Music Minus One. In 1958, Ware was one of 57 jazz musicians to appear in the photograph A Great Day in Harlem. Ware was a member of the Thelonious Monk quartet from 1957 to 1958, he performed with the Sonny Rollins Trio live at the Village Vanguard. Narcotics addiction resulted in his return to a period of incarceration, he was inactive musically for about six years. In 1969, Ware played with Elvin Jones and Sonny Rollins.
He died from emphysema in Philadelphia, Pennsylvania, in 1979. The Chicago Sound with Johnny Griffin With Art Blakey Originally With Tina Brooks The Waiting Game With Sonny Clark Dial "S" for Sonny With Walt Dickerson Tell Us Only the Beautiful Things Walt Dickerson 1976 With Kenny Dorham 2 Horns / 2 Rhythm With Kenny Drew A Harry Warren Showcase A Harold Arlen Showcase I Love Jerome Kern This Is New Pal Joey With Matthew Gee Jazz by Gee With Grant Green Remembering With Johnny Griffin Johnny Griffin Johnny Griffin Sextet Way Out! With Ernie Henry Presenting Ernie Henry Seven Standards and a Blues Last Chorus With Clifford Jordan Jenkins and Timmons ] Starting Time In the World Remembering Me-Me With Herbie Mann The Jazz We Heard Last Summer With Blue Mitchell Big 6 With Thelonious Monk Thelonious Himself Monk's Music Mulligan Meets Monk Thelonious Monk with John Coltrane With J. R. Monterose J. R. Monterose With Lee Morgan Lee Morgan Indeed! With Cecil Payne Zodiac With Rita Reys The Cool Voice of Rita Reys With Sonny Rollins Night at the Village Vanguard With Zoot Sims Zoot!
With Toots Thielemans Man Bites Harmonica! "At Once Old-Timey & Avant-Garde: The Innovation & Influence of Wilbur Ware" Wilbur Ware Discography at www. JazzDiscography.com Down Beat biography Allmusic biography The Wilbur Ware Institute
28S ribosomal protein S29, mitochondrial known as death-associated protein 3, is a protein that in humans is encoded by the DAP3 gene on chromosome 1. This gene encodes a 28S subunit protein of the mitochondrial ribosome and plays key roles in translation, cellular respiration, apoptosis. Moreover, DAP3 is associated with cancer development, but has been observed to aid some cancers while suppressing others; the DAP3 gene encodes a 46 kDa protein located in the lower area of the small mitoribosomal subunit. This protein contains a P-loop motif that binds GTP and a conserved 17-residue targeting sequence responsible for its localization to the mitochondria. Of interest, many of the phosphorylation sites on this protein are conserved and clustered around GTP-binding motifs. Several splice variants were observed in human ESTs that differ in the 5’ UTR region. Pseudogenes for this gene are found in chromosomes 1 and 2. DAP3 is a 28S subunit protein of localizes to the mitochondrial matrix; as part of the mitoribosome, DAP3 participates in the translation of the 13 ETC complex proteins encoded in the mitochondrial genome, in the regulation of cellular respiration.
As a member of the death-associated protein family, DAP3 can be found outside of the mitochondria to initiate the extrinsic apoptotic pathway through its interactions with apoptotic factors, such as tumor necrosis factor-alpha, Fas ligand, gamma interferon. Additionally, DAP3 interacts with the factor IPS-1 to activate caspases 3, 8, 9, resulting in a type of extracellular apoptosis called anoikis. Moreover, DAP3 may contribute to apoptosis through its mediation of mitochondrial fragmentation, as this function extends to the mediation of the oxidative stress response, reactive oxygen species production, mitochondrial homeostasis. DAP3 is essential for life, its deletion in embryos is lethal. Nonetheless, DAP3 and its apoptotic activity can be inhibited by AKT phosphorylation; as aforementioned, death associated protein 3 has regulatory roles in cell respiration and apoptosis. Both opposites and cell respiration are important elements of cell death pathways and have underlying mechanistic roles in ischemia-reperfusion injury.
During a normal embryologic processes, or during cell injury or during developments and processes in cancer, an apoptotic cell undergoes structural changes including cell shrinkage, plasma membrane blebbing, nuclear condensation, fragmentation of the DNA and nucleus. This is followed by fragmentation into apoptotic bodies that are removed by phagocytes, thereby preventing an inflammatory response, it is a mode of cell death defined by characteristic morphological and molecular changes. It was first described as a "shrinkage necrosis", this term was replaced by apoptosis to emphasize its role opposite mitosis in tissue kinetics. In stages of apoptosis the entire cell becomes fragmented, forming a number of plasma membrane-bounded apoptotic bodies which contain nuclear and or cytoplasmic elements; the ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane breakdown and cellular disintegration. Apoptosis occurs in many pathological processes.
It plays an important role during embryonal development as programmed cell death and accompanies a variety of normal involutional processes in which it serves as a mechanism to remove "unwanted" cells. DAP3 has been implicated in numerous cancers. Studies demonstrated that DAP3 expression tended to be low to nonexistent in the tumor cells of B-cell lymphoma, non-small cell lung cancer and neck cancer, breast cancer, gastric cancer, colon cancer due to hypermethylation of the gene’s promoter. Moreover, DAP3 expression has been positively correlated with improved cancer prognosis, indicating that the protein combats cancer progression through its proapoptotic function; as a result, DAP3 could serve as a potential biomarker to monitor the effectiveness of therapeutic treatments such as chemotherapy. However, in other cancers, such as glioblastoma multiforme and thymoma, DAP3 expression was found to be upregulated. Thus, the specific role of DAP3 in various cancers requires further study. DAP3 has been shown to interact with: DELE, IPS-1, AKT, PKA, PKC, NOA1, FADD, Glucocorticoid receptor, Heat shock protein 90kDa alpha, member A1, TNFRSF10A.
PDBe-KB provides an overview of all the structure information available in the PDB for Human 28S ribosomal protein S29, mitochondrial