Disease relevance of Emigration and Immigration

• ELC and EBI1 may thus play roles in migration and homing of normal lymphocytes, as well as in pathophysiology of lymphocytes infected with these herpesviruses [1].
• Erythropoietin promotes MCF-7 breast cancer cell migration by an ERK/mitogen-activated protein kinase-dependent pathway and is primarily responsible for the increase in migration observed in hypoxia [2].
• The E7 phosphoprotein of the nononcogenic HPV-6b, which is generally associated with benign genital warts, is similar to the HPV-16 E7 in amino acid sequence but differs dramatically in migration in sodium dodecyl sulfate-polyacrylamide gels, sedimentation in nondenaturing glycerol gradients, and the ability to bind the RB protein [3].
• Dendritic cells generated from patients with androgen-independent prostate cancer are not impaired in migration and T-cell stimulation [4].
• Loss of calmegin, a testis-specific putative chaperone protein of the endoplasmic reticulum, leads to male sterility because the sperm show defects in migration into the oviduct and do not bind to the zona pellucida [5].

High impact information on Emigration and Immigration

• In vertebrates, insects and nematodes, members of the DCC subfamily of the immunoglobulin superfamily have been implicated as receptors that are involved in migration towards netrin sources [6].
• When these monocyte-derived DCs exit skin to emigrate to LNs, they use not only CCR7 but also CCR8, which was not previously recognized to participate in migration to LNs [7].
• Furthermore, we found that in reeler mutant mice, neuronal precursors accumulated in the olfactory bulb and remained in clusters, indicating that they did not change from tangential chain-migration to radial individual migration [8].
• LFA-1 has a key role in migration to peripheral lymph nodes (pLNs), and influences migration into other LNs [9].
• The alphaEbeta7 integrin appeared to play no role in migration during a primary CD8 T cell immune response in vivo [10].

Biological context of Emigration and Immigration

• We show that eliminating or reducing rho-1 gene function by using a dominant-negative transgene or dsRNA interference results in a severe defect in migration of hypodermal P cells to a ventral position [11].
• Presenilin 1 in migration and morphogenesis in the central nervous system [12].
• FPR-C126W differed from FPR-WT and FPR-F110S in migration on SDS-polyacrylamide gels and tunicamycin-sensitive glycosylation [13].
• However, in some cell types, the increased phosphorylation at S368 did not cause a detectable shift in migration as compared with the nonphosphorylated Cx43 [14].
• On the other hand when we overexpressed a Rack1 variant with alanine substitutions in the putative PKC binding site in its third WD domain, we observed no deficit in migration [15].

Anatomical context of Emigration and Immigration

• These three bands were identical in migration in SDS PAGE to that of the M protein present in freshly prepared crude periplasm [16].
• The role of polysialic acid in migration of olfactory bulb interneuron precursors in the subventricular zone [17].
• To address this issue, we investigated the role of PAK in migration of microvascular endothelial cells [18].
• We explored the hypothesis that the chemotactic migration of carcinoma cells that assemble hemidesmosomes involves the activation of a signaling pathway that releases the alpha6beta4 integrin from these stable adhesion complexes and promotes its association with F-actin in cell protrusions enabling it to function in migration [19].
• The properties of the carboxy-terminal domain of H1 and the possible involvement of the amino acids lysine, proline and alanine in migration are discussed and compared with those of a domain that specifies migration of nucleoplasmin into the oocyte nucleus [20].

Associations of Emigration and Immigration with chemical compounds

• Constitutively increased c-src kinase activity reconstituted the increases in migration and u-PA observed with angiotensin system interruption [21].
• Application of K+ channel blockers (1 and 5 mmol/liter Ba2+, 5 mmol/liter tetraethylammonium, 100 mumol/liter 4-aminopyridine, 5 nmol/liter charybdotoxin) caused marked inhibition of migration, pointing to the importance of K+ channels in migration [22].
• Cells expressing Y397F FAK, which cannot be phosphorylated at a key tyrosine site, showed similar defects in migration pattern and force-induced reorientation as did FAK-null cells [23].
• Digestion with neuraminidase resulted in a shift in migration of the two TGF-beta 1 precursor bands, which suggests that they contain sialic acid residues [24].
• U87 cells treated with S1P showed a significant increase in migration, whereas U118 and U138 cell lines were strongly inhibited [25].

Gene context of Emigration and Immigration

• Cells expressing 18-kD bFGF transfected with a cDNA encoding FGF receptor-2 lacking the COOH-terminal domain (dominant negative bFGF receptor) exhibited a flat morphology and decreases in migration and saturation density [26].
• CXCR4 blockade abrogates their pathology-directed chain migration, a developmentally relevant mode of tangential migration that, if recapitulated, could explain homing along nonstereotypical paths [27].
• In a double-chamber transmigration assay, CD40 activation of MM cells induced a 3-fold (RPMI 8226) and a 5-fold (SV) increase in migration under restrictive, but not permissive, conditions [28].
• The reduction in migration due to p85alpha deficiency in BMMs is associated with reduced adhesion and directed migration on fibronectin and vascular cell adhesion molecule-1 [29].
• We find that dominant negative (N17) versions of Rac and Cdc42 cause a very similar defect in migration as loss of integrins, while those of Rho and Ras have no effect [30].

Analytical, diagnostic and therapeutic context of Emigration and Immigration

• In fact, the percent increase in cAMP level was strongly correlated with the percent decrease in migration activity of SMCs after treatment with adrenomedullin [31].
• Adoptive transfer experiments with CD62L(-/-) CD4(+) T cells prepared from BDC2.5 TCR transgenic mice revealed no apparent defects in migration to pancreatic lymph nodes, proliferation in response to beta cell Ag, or induction of diabetes in NOD.scid recipients [32].
• Ly49D-transfected cells were pretreated with the Syk kinase inhibitor Piceatannol before ligation, which abrogated the previously observed changes in migration toward CXCL10 and CXCL12 [33].
• The decrease in migration rate during pulsed-field gel electrophoresis when BrdU replaces thymidine in the DNA is hypothesized to result from the increase in negative charge on BrdU-labeled DNA [34].
• METHODS: A total of 334 patients treated at the Royal Marsden Hospital (RMH) between 1962 and 1986 with surgery and postoperative radiotherapy were followed up via the NHS Central Register (NHSCR) to identify deaths and emigrations [35].

References