200Pin Memory Ram DRR1 Memory Ram 1G 400MHz PC3200 Memory Ram Module Board for Laptop

Product Information

Ruggeri, J. M. et al. Discoidin domain receptor 1 (DDR1) is necessary for tissue homeostasis in pancreatic injury and pathogenesis of pancreatic ductal adenocarcinoma. Am. J. Pathol. 190, 1735–1751 (2020).

Dudley A, Sater M, Le PU, Trinh G, Sadr MS, Bergeron J et al. DRR regulates AKT activation to drive brain cancer invasion. Oncogene 2014; 33: 4952–4960. Huang Y, Wu M, Li HY . Tumor suppressor ARF promotes non-classic proteasome-independent polyubiquitination of COMMD1. J Biol Chem 2008; 283: 11453–11460. Ambrogio, C. et al. Combined inhibition of DDR1 and Notch signaling is a therapeutic strategy for KRAS-driven lung adenocarcinoma. Nat. Med. 22, 270–277 (2016). Mu P, Nagahara S, Makita N, Tarumi Y, Kadomatsu K, Takei Y . Systemic delivery of siRNA specific to tumor mediated by atelocollagen: combined therapy using siRNA targeting Bcl-xL and cisplatin against prostate cancer. Int J Cancer 2009; 125: 2978–2990. Yoo Y, Wu X, Guan JL . A novel role of the actin-nucleating Arp2/3 complex in the regulation of RNA polymerase II-dependent transcription. J Biol Chem 2007; 282: 7616–7623.

Regulation

Jiang, P. et al. Signatures of T cell dysfunction and exclusion predict cancer immunotherapy response. Nat. Med. 24, 1550–1558 (2018). Li H, Chan L, Bartuzi P, Melton SD, Weber A, Ben-Shlomo S et al. Copper metabolism domain-containing 1 represses genes that promote inflammation and protects mice from colitis and colitis-associated cancer. Gastroenterology 2014; 147: 184–195.e3. Previously, auditors were required to provide an explanation of how they had applied the concept of materiality in planning and performing an audit and they had to specify the overall materiality threshold used (ie materiality for the financial statements as a whole). These disclosures may have included the threshold for performance materiality though this was not a requirement. Huang P, Kishida S, Cao D, Murakami-Tonami Y, Mu P, Nakaguro M et al. The neuronal differentiation factor NeuroD1 downregulates the neuronal repellent factor Slit2 expression and promotes cell motility and tumor formation of neuroblastoma. Cancer Res 2011; 71: 2938–2948.

Kishida S, Mu P, Miyakawa S, Fujiwara M, Abe T, Sakamoto K et al. Midkine promotes neuroblastoma through Notch2 signaling. Cancer Res 2013; 73: 1318–1327. Takahashi Y, Sipp D, Enomoto H . Tissue interactions in neural crest cell development and disease. Science 2013; 341: 860–863. Newman, A. M. et al. Determining cell type abundance and expression from bulk tissues with digital cytometry. Nat. Biotechnol. 37, 773–782 (2019). Lu F, Kishida S, Mu P, Huang P, Cao D, Tsubota S et al. NeuroD1 promotes neuroblastoma cell growth by inducing the expression of ALK. Cancer Sci 2015; 106: 390–396. Almuzzaini B, Sarshad AA, Farrants AK, Percipalle P . Nuclear myosin 1 contributes to a chromatin landscape compatible with RNA polymerase II transcription activation. BMC Biol 2015; 13: 35.Masana M, Su YA, Liebl C, Wang XD, Jansen L, Westerholz S et al. The stress-inducible actin-interacting protein DRR1 shapes social behavior. Psychoneuroendocrinology 2014; 48: 98–110. Mertins, P. et al. Proteogenomics connects somatic mutations to signalling in breast cancer. Nature 534, 55–62 (2016).

Department of Medicine, The Mays Cancer Center, University of Texas Health San Antonio, San Antonio, TX, USA Ashburner, M. et al. Gene ontology: tool for the unification of biology. Nat. Genet. 25, 25–29 (2000). Baarlink C, Wang H, Grosse R . Nuclear actin network assembly by formins regulates the SRF coactivator MAL. Science 2013; 340: 864–867.the UK.). They are also a good way to go if you are looking to retrain and take your life in a brand new direction. Kaur, A. et al. Remodeling of the collagen matrix in aging skin promotes melanoma metastasis and affects immune cell motility. Cancer Discov. 9, 64–81 (2019). Asano Y, Kishida S, Mu P, Sakamoto K, Murohara T, Kadomatsu K . DRR1 is expressed in the developing nervous system and downregulated during neuroblastoma carcinogenesis. Biochem Biophys Res Commun 2010; 394: 829–835. Vogel, W. F. Ligand-induced shedding of discoidin domain receptor 1. FEBS Lett. 514, 175–180 (2002).

Redruth town mayor, Councillor Deborah Reevem said: “This is an excellent show of confidence in the Redruth economy. We welcome the investment into our community and the employment opportunities that this will create.”a) Diagram of full-length (FL) DDR1 (top) and tumour curves of either E0771 Ddr1-WT or KO tumour cells carrying various DDR1 expression vectors: empty vector (EV), FL, deletion of the kinase domain (ΔKD), and extracellular domain (ECD) only. All p values were compared to KO + EV group. TM: transmembrane domain. WT: n = 9 tumours, KO+EV: n = 10 tumours, KO+FL: n = 10 tumours, KO+ ΔKD: n = 6 tumours, KO+ECD: n = 5 tumours. ( b) Crystal structure of mouse DDR1 collagen-binding domain, generated by Jmol software ( http://www.jmol.org/). Amino acid residues targeted in the mutational analysis are shown. ( c) Immunoblots of Flag-tagged mouse WT DDR1-ECD and point mutants ectopically expressed in M-Wnt tumour cells, with GAPDH as the loading control. Images are representatives from three independent experiments. ( d) Immunoblots of Flag-tagged mouse WT DDR1-ECD and point mutants ectopically expressed in AT-3 tumour cells, with GAPDH as the loading control. Images are representatives from three independent experiments. ( e–f) Growth curves of M-Wnt (e) and AT-3 (f) Ddr1-KO tumours with ectopically expressed mouse WT DDR1-ECD or collagen-binding point mutants. The numbers in parenthesis indicate outgrowing tumours (larger than 100 mm 3) versus total injected. ( g, h) Immunoblots of full-length DDR1 in cells and soluble ECD in conditioned medium from various mouse (g) and triple-negative human breast cancer cell lines plus ER-positive MCF7 (h). Images are representatives from three independent experiments. ( i) Coomassie staining of recombinant Fc-ECD under non-reducing and reducing conditions. ( j) Rescue of Ddr1-KO E0771 tumour growth in immunocompetent hosts by recombinant Fc-ECD versus PBS vehicle (n = 6 tumours/group). ( k) Diagram of the Transwell assay for CD8 + T cell migration. Primary CD8 + T cells were loaded in the upper chamber that had been pre-seeded with decellularized ECM derived from tumour cells. The lower chamber contained medium with or without CCL21. ( l) CD8 + T cells in vitro migration activity was abrogated by decellularized ECM from AT-3 tumour cells in a DDR1-dependent manner. Value of migrated CD8 + T cell number without ECM and CCL12 is set at “1” (lanes 1 and 2: n = 3; lanes 3 and 4: n = 7), n refers to technical repeats. Values represent mean ± SEM. p value as indicated, two-tailed Student’s t-test for all tests except for tumour volumes, which were done by two-way ANOVA. Salmon, H. et al. Matrix architecture defines the preferential localization and migration of T cells into the stroma of human lung tumors. J. Cell. Invest. 122, 899–910 (2021). Agarwal, G., Mihai, C. & Iscru, D. F. Interaction of discoidin domain receptor 1 with collagen type 1. J. Mol. Biol. 367, 443–455 (2007). Leitinger, B. Discoidin domain receptor functions in physiological and pathological conditions. Int. Rev. Cell Mol. Biol. 310, 39–87 (2014). a) E0771 Ddr1-WT/KO tumours transplanted from Rag1 −/− to C57BL/6 hosts were analysed by SHG, To-pro-3 staining for all nuclei, and collagen fibre individualization. Scale bar: 50 µm. ( b, c) M-Wnt (WT n = 8 tumours, KO n = 4 tumours) and AT-3 (n = 5 tumours/group) Ddr1-WT/KO tumours transplanted from Rag1 −/− to C57BL/6 hosts were analysed for infiltrating CD3 + T cells normalized by total cells via IHC. ( d–g) M-Wnt and AT-3 Ddr1-WT/KO tumours transplanted from Rag1 −/− to C57BL/6 hosts were analysed for collagen fibre alignment (d, e) and fibre length (f, g), n = 4 tumours/group. ( h–j) E0771, n = 5 tumours/group (h), M-Wnt, n = 4 tumours/group (i) and AT-3, n = 4/group (j) Ddr1-WT/KO tumours transplanted from Rag1 −/− to C57BL/6 hosts were analysed for fibre numbers by the CT-Fire software. ( k–m) E0771 Ddr1-WT/KO tumours (WT n = 10 tumours, KO n = 8 tumours) from immunodeficient Rag1 −/− hosts were analysed for collagen fibre alignment (k), fibre length (l) and fibre numbers (m) by the CT-Fire software. ( n) Growth curves of E0771 Ddr1-KO tumours in immunocompetent hosts that were intratumorally injected with recombinant WT and mutant Fc-ECD (WT: n = 10 tumours, W54A: n = 9 tumours). ( o) Representative images of E0771 Ddr1-KO tumours treated with recombinant WT or mutant Fc-ECD in C57BL/6 hosts as analysed by SHG, To-pro-3 staining, and collagen fibre individualization. Scale bar: 50 µm. ( p) Quantification of collagen fibre alignment in WT and mutant Fc-ECD treated tumours (n = 5 tumours/group). ( q) Enumeration of infiltrating CD3 + T cells normalized by total cells via IHC (WT: n = 4 tumours, KO: n = 3 tumours). Values represent mean ± SEM. p value as indicated, two-tailed Student’s t-test for all tests except for tumour volumes, which were done by two-way ANOVA.