Dirk M. Anderson's research while affiliated with Molecular and Cellular Biology Program and other places

... It generates trans-phosphorylation in the JMD region, kinase insert region, KD, and COOH-terminal tail ( Figure 1B) [3,18,19]. The signals transmitted by KIT activation are primarily mediated through the phosphatidylinositol 3-kinase (P13K) pathway [20,21], Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway [22][23][24], MAPK pathway [25][26][27], and the Src family kinase pathway [26,28] (Figure 1C). In the hematopoietic system, KIT is strongly expressed in hematopoietic stem cells and progenitor cells [29]. ...

... Zhuravko et al., 2015 optimized the solubilization of IFN␤1b from inclusion bodies, using different solvents like ethanol, 1-propanol, and 2-propanol at their different concentrations in aqueous solutions. They found 55% propyl alcohol solution to be the best solvent for IFN␤1b solubilization as it enabled them to extract 85-90% of the target protein from inclusion bodies [242]. Acetic and butyric acid (5-80%) are used to solubilize IL-2 and IFN␤, respectively [243]. ...

... Moreover, a comparatively lower level of SCF, particularly in GSK-3β overexpressing cells undergoing hypoxia, indicates that GSK-3β further suppresses SCF expression, post-MI. SCF has limited efficacy alone, but when mixed with other growth factors such as GM-CSF and EPO, it displays a synergistic effect, particularly on hematopoietic stem cells (Bernstein et al., 1991;Williams et al., 1992). We observed that GSK-3β attenuates the levels of both GM-CSF and EPO, along with SCF, in cardiomyocytes post-hypoxia and, observed increased number of CPCs in the cKO post-MI in this study is a possible synergistic paracrine effect of different growth factors. ...

... Among these are the levels of CD40 and its ligand CD40L, both of which were negatively associated with TOMM40 levels in many tumors such as BLCA, LUSC, PRAD, and SKCM. The interactions between CD40 and CD40L stimulate B cells to secret cytokines and also activate T cells to attack and kill malignant cells (Kooten and Banchereau 2000; Armitage et al. 1992). In addition, levels of CD28 (which is critical for the costimulation of naive T lymphocytes and regulation of T cells) were also negatively associated with TOMM40 levels (Lenschow et al. 1996;Bour-Jordan et al. 2011;Salomon and Bluestone 2001). ...

... We considered the possibility that the abundance of hematopoietic growth factors displayed on WT and cKO niche cells may differ 8,43 . Of note, SCF is particularly attractive given its critical role in HSC homeostasis, survival, and proliferation, and the fact that mSCF is particularly important for hematopoiesis [44][45][46] . Although transcript levels for SCF (Kitl) did not reveal differences between cKO and control Lepr+ MSPCs (Fig. 6a), we detected a significant increase in mSCF on bone marrow Lepr + MSPCs and ECs (Fig. 6b-d). ...

... KIT signaling is known to promote cell survival, proliferation, and differentiation in a variety of processes including gametogenesis, melanogenesis, and hemopoiesis [13,14]. The transmembrane receptor, KIT, and its ligand KITL or stem cell factor (SCF), are encoded by the murine White spotting (W) and Steel (Sl) loci, respectively [15][16][17][18][19][20]. Loss of KIT function in W or Sl mutants impairs PGC migration and proliferation, and affects the growth of ovarian follicles [21][22][23]. ...

... A second strategy involves blocking death receptor signalling. One of the earliest documented viral escape mechanisms involves the Shope fibroma virus, which secretes TNF-R2 homologues, neutralizes TNF-α and inhibits cell apoptosis [24]. Finally, another prominent mechanism by which viruses inhibit cell apoptosis is by inhibiting the activity of caspases. ...

... The blockade of these contact-dependent signals, by anti-IL30 neutralizing Abs, hinders proliferation and self-renewal of hBCSCs, suggesting IL30's ability to control the maintenance and expansion of the CSC compartment. Therefore, IL30 enters the group of human membrane-anchored cytokines, which includes IL1α, 38 IL15, 39 M-CSF, 40 Flt3 ligand, 41 TNFα, 42 LTα, 43 Fractalkine/CX3CL1, 44 TGFβ 45 and IFNγ, 46 that have demonstrated biological effects via the juxtacrine route, under physiological conditions. Signaling through cell-cell contact, IL30 overexpressed by hBCSCs triggers a storm of inflammatory mediators, including IL1β, TNFα, CCL4, CXCL8, CXCL10 and, especially, CSF2/GM-CSF, CXCL1, IL23A and CXCL10. ...

... As the indicator of the Th17 response, IL-17A was not detected in the cell culture supernatant following AST VII treatment in 1/20 diluted hWB, possibly resulting from the consumption of IL-17A via IL-17 receptor. This consumption by a specific receptor in vitro has also been suggested as the possible reason for undetectable IL-4 in cell culture supernatant [38,39]. ...

... Mast cells are capable of producing several mediators that stimulate the proliferation of melanocytes (8,15,16). The increased levels of cell-free SCF in lesional skin of mastocytosis patients can also enhance melanocytosis (17). On the contrary, wild-type mast cells can probably inhibit the progression and invasion of melanomas (18,19). ...