Joe Sumner's sister Fuchsia Sumner is an actress. Joe Sumner Has Five Siblings Fuchsia Sumnerįuschia Kate in a black bodycon dress and multilayered chain.( Source : Over the years, they have welcomed three children. The singer fell in love with Styler at the very first meeting itself in 1977, Sumner penned in his autobiography titled Broken Music.įollowing Sumner and Tomelty's divorce, Tyler and Sting tied the knot on August 20, 1992, at Camden Registry Office. Sting and Trudie Styler on a long and successful marriage ( Source : youtube ) In fact, Trudie lived next door to the couple in Bayswater, west London. Their separation was quite controversial for Styler was Tomelty's best friend. Later, they divorced following the disclosure of Sting's relationship with Trudie Styler. Unfortunately, the couple separated after welcoming their second child daughter Fuschia. They were married for eight years before they divorced in 1984.įrances, a notable actress, and Sting walked down the aisle on May 1, 1976. Joe was born to Sting and Frances on November 23, 1976. Let alone, Joseph, all of his brothers and sisters also belong to the entertainment industry. Joe followed in the steps of his father into the music industry. He is widely recognized as the frontman of The Police. Gordon Matthew Thomas Sumner CBE, better known as Sting is a remarkable English singer. Joe is the son of the celebrated musician.įather and son duo, Sting (left) and Joe Sumner (right)( Source : However, only Fuschia Katherine and Joe are full siblings. These results suggest the therapeutic potential of ASOs in Usher syndrome and other diseases of the ear and eye.Joe Sumner family includes parents Sting and Frances Tomelty and five siblings. Our results show that ASOs can effectively target Ush1c mutations both in vitro and in vivo. Treatment with 216A-targeted ASOs to neonate mice corrected protein expression with an improvement in harmonin localization in the hair cells and photoreceptors rescued vestibular and hearing function, and demonstrated a small improvement in visual function. Cell-free and cellular assays also demonstrated that ASOs targeted to the Ush1c.238dupC mutation result in in-frame skipping of exon 3. Visual function was evaluated by electroretinogram (ERG) analyses and optical coherence tomography (OCT) imaging was used to examine ocular structures.ĪSOs effectively corrected splicing of 216A RNA in an Usher patient cell line, and in the cochleae and retinas of 216AA mice when delivered systemically or locally. Hearing and vestibular function were evaluated by auditory-evoked brain stem response (ABR) and open-field chamber analysis, respectively. Immunofluorescence was used to analyze Harmonin expression and ASO localization. Correction of splicing was evaluated by RT-PCR and western blot. This mouse model provides an opportunity to test the feasibility of correcting the disease-associated genetic defect using antisense oligonucleotides (ASOs).Īntisense oligonucleotides (ASOs) were used to target Ush1c mutations in vitro and in vivo by systemic or local injection. 216AA mice exhibit circling behavior indicative of severe vestibular dysfunction and deafness, have retinal dysfunction by 1 month of age and begin to lose photoreceptors after 6 months of age. We created a mouse model for Usher 1C by knocking in the 216A mutation. The 216G>A (216A) mutation in USH1C creates a cryptic splice site that is used preferentially over the correct site and results in a truncated harmonin protein. Type 1 Usher (Usher 1) is characterized by profound hearing impairment and vestibular dysfunction at birth, and the development of retinitis pigmentosa (RP) in early adolescence. Usher syndrome (Usher) is the leading genetic cause of combined deafness and blindness.
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