TXK

Description

The TXK (TXK tyrosine kinase) is a protein-coding gene located on chromosome 4.

TXK (Telephone eXchange Crossbar) was a series of Crossbar exchanges used by the British Post Office telephone network, subsequently BT, between 1964 and 1994. TXC was used as the designation at first, but this was later changed as TXC sounded too much like TXE the code used for later electronic exchanges. Prior to this the GPO had standardised on Strowger for automatic switching and had resisted the adoption of Crossbar, preferring to wait for its electronic switching research to bear fruit. The development of electronic systems however took longer than anticipated and the British equipment manufacturers, particularly Automatic Telephone & Electric (ATE), which later became part of the Plessey group feared that continuing to focus the bulk of their production on Strowger equipment would harm their export sales as Crossbar had already become popular throughout the world. In response to this, ATE, and later Plessey, developed their own crossbar system, the 5005, and pushed for the GPO to adopt it as an interim measure. Normally the GPO preferred to develop systems in co-operation with the manufacturing companies, from whom they could then purchase competitively rather than allowing one manufacturer to sell it a proprietary system. The situation however was becoming critical, waiting lists for telephone service in the UK were growing embarrassingly long and the manufacturers were becoming more and more reluctant to supply Strowger in the quantities needed by the GPO. Eventually the GPO relented and decided to accept Crossbar equipment into its network.

== TXK1 == This code was given to Plessey's 5005A switch, which was used for local exchanges in non-director areas or group switching centres / sector switching centres (tandem exchanges). The 5005A was a two wire version of the 5005, meaning the transmit and receive speech was routed through the switch over one pair of wires. The first one was installed at Broughton, Preston, in 1964 as a field trial replacing Broughton's manual exchange.

TXK is a non-receptor tyrosine kinase that plays a redundant role with ITK in regulating the adaptive immune response. It is involved in the development, function, and differentiation of conventional T-cells and nonconventional NKT-cells. Upon activation of the T-cell receptor (TCR) by antigen-presenting cells (APC), TXK is recruited to the cell membrane and phosphorylated at Tyr-420, leading to its full activation. TXK participates in signaling from various receptors and contributes to multiple downstream pathways, including the regulation of the actin cytoskeleton. Similar to ITK, TXK can phosphorylate PLCG1, resulting in its localization in lipid rafts and activation, followed by the cleavage of its substrates. This process triggers calcium release from the endoplasmic reticulum into the cytoplasm and the translocation of the nuclear activator of activated T-cells (NFAT) into the nucleus for transcriptional activity. TXK plays a role in the positive regulation of IFNG transcription in T-helper 1 cells as part of an IFNG promoter-binding complex with PARP1 and EEF1A1. Within this complex, TXK phosphorylates both PARP1 and EEF1A1. TXK also phosphorylates key sites in LCP2, leading to the up-regulation of the Th1 preferred cytokine IL-2. Additionally, TXK phosphorylates 'Tyr-201' of CTLA4, promoting the association of PI-3 kinase with the CTLA4 receptor.

TXK is also known as BTKL, PSCTK5, PTK4, RLK, TKL.

Associated Diseases

WES Whole Exome Sequencing