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SLP76 (SH2 domain-containing leukocyte protein of 76 kDa) is a cytosolic adaptor protein which translocates to the plasma mambrane and is involved in multiple signaling pathways in T cells, mast cells, neutrophils and platelets; B cells express its analog SLP65/BLNK (B cell linker protein). SLP76 is phosphorylated by Syk-family and Tec-family tyrosine kinases and couples them to the phosphorylation and activation of PLC-gamma. Via Gads or Grb2, SLP76 also associates with LAT adaptor by involvement of SLP76 proline-rich region. The SH2 domain of SLP76 has been identified as the region involved in binding the serine/threonine kinase HPK1. HPK1 may act as both a positive and a negative regulator by promoting the Jnk-mitogen activated protein kinase (MAPK) pathway and inhibiting the pathway leading to AP-1 activation ...
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Mammalian Nck1 and Nck2 are closely related adaptor proteins that possess three SH3 domains, followed by an SH2 domain, and are implicated in coupling phosphotyrosine signals to polypeptides that regulate the actin cytoskeleton. However, the in vivo functions of Nck1 and Nck2 have not been defined. We have mutated the murine Nck1 and Nck2 genes and incorporated β-galactosidase reporters into the mutant loci. In mouse embryos, the two Nck genes have broad and overlapping expression patterns. They are functionally redundant in the sense that mice deficient for either Nck1 or Nck2 are viable, whereas inactivation of both Nck1 and Nck2 results in profound defects in mesoderm-derived notochord and embryonic lethality at embryonic day 9.5. Fibroblast cell lines derived from Nck1−/− Nck2−/− embryos have defects in cell motility and in the organization of the lamellipodial actin network. These data suggest that the Nck SH2/SH3 adaptors have important functions in the development of mesodermal ...
The adaptor protein Src homology 2 domain-containing leukocyte phosphoprotein of 76 kDa (SLP-76) plays a crucial role in T cell activation by linking antigen receptor (T cell receptor, TCR) signals to downstream pathways ...
This gene encodes the substrate of breast tumor kinase, an Src-type non-receptor tyrosine kinase. The encoded protein possesses domains and several tyrosine phosphorylation sites characteristic of adaptor proteins that mediate the interactions linking proteins involved in signal transduction pathways. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2008 ...
KARAP/DAP12/TYROBP: three names and a multiplicity of biological functions.: The signaling adaptor protein KARAP/DAP12/TYROBP (killer cell activating receptor-a
Article Stap-2 negatively regulates both canonical and noncanonical nf-b activation induced by epstein-barr virus-derived latent membrane protein 1. The signal-transducing adaptor protein 2 (STAP-2) is a recently identified adaptor protein that conta...
The adhesion and degranulation adaptor protein (ADAP) was initially identified as a molecular adapter that couples T cell receptor (TCR) stimulation to the avidity of integrins governing T cell adhesion. TCR stimulation promotes the formation of a multi-protein complex containing CARMA1, MALT1, and BCL-10, which through the association of ADAP, ultimately activates the NF-kappaB family of transcription factors. More recent experiments have shown that ADAP controls optimal T cell proliferation, cytokine production, and expression of the Bcl-2 family member Bcl-x(L), suggesting that ADAP regulates T cell activation by promoting antigen-dependent T cell-antigen presenting cell (APC) activation. At least three isoforms of ADAP are known to exist ...
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Identification and characterization of the hematopoietic cell-specific enhancer-like element of the mouse hex gene.: Hex is one of the homeobox genes suggested
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The KOMP Repository is located at the University of California Davis and Childrens Hospital Oakland Research Institute. Question? Comments? For Mice, Cells, and germplasm please contact us at [email protected], US 1-888-KOMP-MICE or International +1-530-752-KOMP, or for vectors [email protected] or +1-510-450-7917 ...
ECSIT兔多克隆抗体(ab21288)可与小鼠, 人样本反应并经WB, IP, IHC, ICC/IF实验严格验证,被9篇文献引用。所有产品均提供质保服务,中国75%以上现货。
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Most difficulties in working with Micro-Manager arise from configuring the system and from problems/issues with specific devices. In both of these cases you are interacting mainly with device adapters. These device adapters have been written by several different authors, all behave slightly differently, and interact with specific hardware that has its own peculiarities. On these pages we will maintain as much information as possible about Micro-Manager device adapters. This will help you configure and understand your Micro-Manager system. We hope that the authors of the device adapters will maintain this information, but please feel free to update the information here with your own experiences. The information here will refer to the most recent Micro-Manager release. ...
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- Please make sure the part number, series number and model number are all matching your original adapter. Model : PCGA-AC19V3 Input :
Please make sure the part number Please make sure the part number, series number and model number are all matching your original adapter.
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Adaptor proteins are essential components of T cell receptor (TCR) signaling cascades regulating gene transcription and cytoskeletal reorganization. The molecular adaptor adhesion- and degranulation-promoting adaptor protein (ADAP), also known as Fyn binding protein (FYB) or Slp-76-associated protein of 130 kilodaltons (SLAP-130), interacts with a number of signaling intermediates including Slp-76, the Src family tyrosine kinase Fyn, vasodilator-stimulated phosphoprotein (VASP), and the actin-nucleating protein WASP. Recently ADAP was shown genetically to positively regulate T cell activation, TCR-induced integrin clustering, and T cell adhesion. The mechanism by which ADAP couples TCR stimulation to integrin clustering remains unclear; however, studies of ADAP, the exchange factor Vav1, and WASP suggest that TCR and integrin clustering may be controlled by distinct signaling pathways.. ...
N-Myristoylated ubiquitin ligase Cbl-b inhibitor prevents on glucocorticoid-induced atrophy in mouse skeletal muscleN-Myristoylated ubiquitin ligase Cbl-b inhibitor prevents on glucocorticoid-induced atrophy in mouse skeletal muscle ...
Signal Transducing Adaptor Proteins: A broad category of carrier proteins that play a role in SIGNAL TRANSDUCTION. They generally contain several modular domains, each of which having its own binding activity, and act by forming complexes with other intracellular-signaling molecules. Signal-transducing adaptor proteins lack enzyme activity, however their activity can be modulated by other signal-transducing enzymes
Mammalian cell membranes provide an interface between the intracellular and extracellular compartments. It is currently thought that cytoplasmic signaling adapter proteins play no functional role within the extracellular tumor environment. Here, by selecting combinatorial random peptide libraries in tumor-bearing mice, we uncovered a direct, specific, and functional interaction between CRKL, an adapter protein [with Src homology 2 (SH2)- and SH3-containing domains], and the plexin-semaphorin-integrin domain of beta(1) integrin in the extracellular milieu. Through assays in vitro, in cellulo, and in vivo, we show that this unconventional and as yet unrecognized protein-protein interaction between a regulatory integrin domain (rather than a ligand-binding one) and an intracellular adapter (acting outside of the cells) triggers an alternative integrin-mediated cascade for cell growth and survival. Based on these data, here we propose that a secreted form of the SH3/SH2 adaptor protein CRKL may act ...
The Tec-family protein tyrosine kinase IL-2-inducible T cell kinase (ITK) mediates T cell activation, as does the adaptor protein SLP-76 (SH2-domain-containing leukocyte protein of 76 kD), which forms a complex with ITK and other intracellular signaling enzymes. One of these enzymes is phospholipase C-γ1 (PLC-γ1), which mediates T cell receptor (TCR)-stimulated intracellular calcium mobilization leading to the activation of transcription factors such as nuclear factor of activated T cells. The Src-family tyrosine kinase Lck and the Syk-family tyrosine kinase ζ chain-associated protein kinase of 70 kD (ZAP-70), together with ITK, are necessary for the phosphorylation of PLC-γ1 in response to TCR stimulation. ITK is thought to phosphorylate a specific tyrosine residue of PLC-γ1 that is required for its activation. The mechanism of activation of ITK appears to involve the interaction between SLP-76 and ITK, which not only initiates ITK activity but is also important to maintain the kinase ...
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
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J. Biotechnol. 126, 463-474 (2006). Maruoka M*, Suzuki J*, Kawata S, Yoshida K, Hirano N, Sato S, Goff SP, Takeya T, Tani K and Shishido T. *equal contribution Identification of B cell adaptor for PI3-kinase (BCAP) as an Abl interactor 1-regulated substrate of Abl kinase ...
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Orderly progression through the cell cycle is essential to maintain ploidy and stability of the genome. For the transition from G2 into mitosis, upstream checkpoint proteins signal the timing of mitotic entry. Among these are checkpoints to detect completion of DNA replication, the absence of genomic lesions, the doubling of cell mass, and the synthesis of macromolecules. Ultimately, these signals up- or downregulate the inhibitory Y15 phosphorylation of Cdc2, the universal switch for the transition from G2 into mitosis. Through controlling the kinases and phosphatases that phosphorylate and dephosphorylate Y15, these checkpoint-signaling pathways work together to ensure that mitosis is initiated only when it will result in two viable and identical daughters. Although most checkpoints halt cell cycle progression in response to an insult, osmotic stress and limited nutrition actually advance mitotic entry in S. pombe (Young and Fantes 1987; Shiozaki and Russell 1995). It is therefore likely that ...
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In this paper, Scheinfeld and colleagues from the DAdamio laboratory extended their work on the interaction between JIP-1 and APP. JIP is JNK-interacting protein-1, which several groups, including the DAdamio lab, last year showed to bind to the cytoplasmic tail of APP. Those labs showed that JIP-1 interacted with APP and that overexpression of JIP-1 altered APP processing and metabolism (principally dealing with APP phosphorylation and secretion and Aβ release).. An area of APP biology that has taken center stage recently is the potential role in nuclear signal transduction. This idea has been too inviting by analogy to Notch signaling ever since γ-secretase was shown to cleave both APP and Notch, the latter to generate the nuclear signaling-competent NICD fragment. Evidence has been building in the last two years that the APP cognate of NICD, coined AID or AICD, indeed has signaling properties. First shown in a reporter system by Cao and Sudhof, this observation was confirmed by the ...
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p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
In this study, we have shown that a mutant CIKS protein lacking the N-terminal TRAF6 binding domain significantly impaired IL-17-induced expression of target genes, but had no impact on the response to IL-17 plus TNF-α. This was the case even though the genetic response to IL-17 plus TNF-α included genes that were induced by IL-17, but not TNF-α; furthermore, these genes were induced by IL-17 in manner dependent on the TRAF6 recruitment domain of CIKS. Importantly, among the proteins encoded by these latter genes were transcription factors such as IκBζ and C/EBPδ, which in turn are involved in the expression of later-induced genes in response to both IL-17 and IL-17 plus TNF-α. Therefore, our results may be extrapolated to suggest that the overall genetic response to IL-17 plus TNF-α appears to be largely unaffected by loss of the TRAF6 recruitment domain in CIKS. Consequently, such a mutant CIKS adaptor would not be expected to interfere with IL-17-mediated contributions in an ...
Oligonucleotide sequences for TruSeqTM RNA and DNA Sample Prep Kits1 TruSeq Universal Adapter 5 AATGATACGGCGACCACCGAGATCTACACTCTTTCCCTACACGACGCTCTTCCGATCT TruSeq Adapters barcode: ATCACG TruSeq Adapter, Index 1 5 GATCGGAAGAGCACACGTCTGAACTCCAGTCACATCACGATCTCGTATGCCGTCTTCTGCTTG TruSeq Adapter, Index 2 5 GATCGGAAGAGCACACGTCTGAACTCCAGTCACCGATGTATCTCGTATGCCGTCTTCTGCTTG TruSeq Adapter, Index 3 5 GATCGGAAGAGCACACGTCTGAACTCCAGTCACTTAGGCATCTCGTATGCCGTCTTCTGCTTG TruSeq Adapter, Index 4 5 GATCGGAAGAGCACACGTCTGAACTCCAGTCACTGACCAATCTCGTATGCCGTCTTCTGCTTG TruSeq Adapter, Index 5 5 GATCGGAAGAGCACACGTCTGAACTCCAGTCACACAGTGATCTCGTATGCCGTCTTCTGCTTG TruSeq Adapter, Index 6 5 GATCGGAAGAGCACACGTCTGAACTCCAGTCACGCCAATATCTCGTATGCCGTCTTCTGCTTG TruSeq Adapter, Index 7 5 GATCGGAAGAGCACACGTCTGAACTCCAGTCACCAGATCATCTCGTATGCCGTCTTCTGCTTG TruSeq Adapter, Index 8 5 GATCGGAAGAGCACACGTCTGAACTCCAGTCACACTTGAATCTCGTATGCCGTCTTCTGCTTG TruSeq Adapter, Index 9 5 GATCGGAAGAGCACACGTCTGAACTCCAGTCACGATCAGATCTCGTATGCCGTCTTCTGCTTG ...
To clarify things a bit more here in the post though, let me provide a bit more detail on what goes into my VMs network configuration. In VBox Manager -, pfSense VM -, Settings -, Network, Adapter 1 is a Bridged Adapter and Adapter 2 is a Host-Only Adapter. Under the USB Settings, I have a USB Device Filter configured to match my Alfa USB WiFi adapter. These are all the configured devices that will eventually become the actual network interfaces in pfSense once the VM boots. During the VM boot process, the pfSense kernel detects Network Adapter 1 as /dev/em0, Network Adapter 2 as /dev/em1 and the USB WiFi adapter as /dev/run0. Later in the boot process, pfSense configures these network devices as network interfaces typical for a network router. In my case, the VM Bridged adapter (em0) becomes the WAN interface where all Internet-bound traffic is directed. Since pfSense provides a GUI for configuration, the VM Host-Only adapter (em1) becomes a LAN interface (192.168.56.2/24) which allows ...