Publication for ITGAL and SELPLG

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	ITGAL	integrin subunit alpha L	3683			[link]
hsa	SELPLG	selectin P ligand	6404

Pubmed ID	Priority	Text
23834268	0.98	CD11a, CD31, CD62L and CD162 was reduced on sputum neutrophils compared to blood neutrophils.
	0.97	CD162, no differences in CD11a and CD62L and both increased and unchanged CD11b on neutrophils in COPD.
	0.96	CD11a (Panel A), CD11b (Panel B), CD31 (Panel C), CD162 (Panel D), CD62L (Panel E), CD54 (Panel F), CD63 (Panel G), CD66b (Panel H).
	0.96	CD11a, CD11b, CD62L and CD162 was reduced compared to baseline values on days 5-12 post-inoculation, followed by recovery to baseline levels.
	0.96	CD11a, CD31, CD162 and CD62L on sputum neutrophils.
	0.96	CD11a on peripheral blood neutrophils was reduced in both COPD and non-COPD subjects, and CD11b, CD62L and CD162 were significantly reduced in COPD subjects only.
	0.96	CD11a, CD11b, CD62L and CD162 on peripheral blood neutrophils following rhinovirus infection in COPD subjects, and correlations between CD11b and exacerbation severity.
	0.93	CD11a (Panel A), CD11b (Panel B), CD162 (Panel C) and CD62L (Panel D).
	0.91	CD162 (mediating initial steps of neutrophil rolling and capture), CD11a and CD11b (required for firm neutrophil adhesion), CD31 and CD54 (involved in neutrophil transmigration through the endothelial monolayer) and CD63 and CD66b (neutrophil activation markers).
24115949	0.98	CLA), an inducible carbohydrate modification of PSGL-1, CCR4, CCR8, CCR10, alpha4beta1, and LFA-1, which mitigates their migration into the skin.
	0.91	PSGL-1, S1P1, and the integrins LFA-1 and/or alpha4beta1 (VLA-4) as well as other integrins that engage the extracellular matrix (ECM).
22701459	0.96	PSGL-1 signaling results in the conversion of LFA-1 from an inactive state to an extended conformation that then interacts with ICAM-1 to reduce neutrophil rolling velocity.
	0.96	PSGL-1 and CXCR2 signaling pathways that regulate LFA-1 activation contribute to neutrophil adhesion and recruitment.
	0.96	LFA-1 extension and not conversion to the high affinity state, why does CXCR2 engagement lead to neutrophil behavior qualitatively distinct from the PSGL-1 pathway that has also been shown to induce LFA-1 extension?
	0.95	PSGL-1 signaling seems to induce only the extended conformation of LFA-1, and even pulling on LFA-1 as it transiently engages with ICAM-1 in slow rolling is not sufficient to induce rapid neutrophil arrest mediated by the high affinity conformation.
	0.89	PSGL-1 transduces an intracellular signal that partially activates LFA-1 (; Figure 2).
	0.88	PSGL-1, it seems that ligation of PSGL-1 triggers LFA-1 extension only in myeloid cells.
	0.88	LFA-1 activation, whereas PSGL-1 signals to LFA-1 may not be as spatially confined.
	0.73	PSGL-1 signals talin-1-dependent LFA-1 extension, whereas chemokine GPCRs signal LFA-1 activation to a high affinity state that requires both talin-1 and Kindlin-3.
	0.71	LFA-1 engages ICAM-1 during slow rolling interactions induced by PSGL-1 signaling.
	0.57	LFA-1 extension resulting in distinct slow rolling and arrest behaviors after PSGL-1 and CXCR2 signaling, respectively, may be that chemokines also stimulate an increase in LFA-1 mobility in the membrane that could lead to ligand-driven LFA-1 clustering and subsequent firm adhesion.
24113789	0.96	PSGL-1 (n=11) and L-selectin (n=9) and ~ 1.3 x 10-10 cm2/s for both LFA-1 (n=9) and Mac-1 (n=9) (Figure 4).
	0.95	PSGL-1 is more closely related to LFA-1, FRAP and our new ICM measurements show PSGL-1 membrane mobility is much different from LFA-1 and almost identical to L-selectin.
	0.91	PSGL-1 having different membrane dynamics from LFA-1.
	0.89	LFA-1, PSGL-1 and Mac-1.
	0.88	PSGL-1) is significantly lower than the mobility of integrins, LFA-1 (alphaLbeta2) and Mac-1 (alphaMbeta2), in the resting cell.
27338562	0.96	PSGL-1) and late (LFA-1, VLA-4 and alphaVbeta3) adhesion molecules was evaluated in U937 cells on a time course (3-24 h) using a wide range of concentrations (0.001-100 mug/mL) of three types of TiO2 NPs (<25 nm anatase, 50 nm anatase-rutile or < 100 nm anatase).
	0.96	PSGL-1, LFA-1, VLA-4 and alphaVbeta3, promoting the adhesion of monocytes to endothelial cells, even if these endothelial cells were not challenged with particles.
	0.95	PSGL-1 as early as 3 h (Fig. 1a-d), after exposure and LFA-1, VLA-4 and alphaVbeta3 as early as 8 h after exposure (Additional file 1), reaching a peak 18 h after exposure (Fig. 2 a-f).
	0.89	PSGL-1 (P-selectin ligand), LFA-1 (ICAM-1 ligand), VLA-4 (VCAM-1 ligand) and alphaVbeta3 (PECAM-1 ligand), among others.
	0.69	PSGL-1 (up to 3-fold of the positive controls) and after 18 h of exposure for LFA-1, VLA-4 and alphaVbeta3 (up to 2.5-fold of the positive controls).
29353325	0.96	PSGL-1 occurs within mutual lipid raft domains to mediate signalling to Src family kinases and trigger LFA-1 (alphaLbeta2, CD11a/CD18) integrin activation (Stadtmann et al.).
	0.96	PSGL-1, which exposed the contribution of L-selectin-dependent modulation of LFA-1 activity.
19667063	0.96	cutaneous lymphocyte-associated antigen (CLA), CC chemokine receptor 4 (CCR4), a chemokine receptor found on skin homing T cells, and CD11a, which is essential for firm adhesion to endothelium via interaction with the beta2-integrin intercellular adhesion molecule-1 (ICAM-1), on CD4+ T cells from old and young individuals.
21060818	0.95	PSGL-1 and CD43 and the non-uropod marker LFA-1.
19594629	0.92	PSGL-1, LFA-1 or LPAM-1.
23994464	0.92	PSGL-1 and also triggers an intermediate-affinity conformational state of the beta2-integrin LFA-1 on neutrophils (Fig. 3).
23278740	0.91	PSGL-1 and LFA-1-ICAM-1 associations.
27602371	0.88	PSGL-1 leads to further neutrophil activation of the beta2-integrins, CD11a/CD18, LFA-1 (alphaLbeta2), CD11b/CD18 and Mac-1 (alphaMbeta2) that do not require additional stimuli, which result in massive neutrophil migration and accumulation in distal organs such as lung and liver to cause tissue injury.
30944838	0.84	LFA-1 binding to ICAM-1 initiates a change in neutrophil motion from rolling to adhesion, while the activation of LFA-1 depends on signals from PSGL-1 and CD44.
9091586	0.79	CLA+ cells from normal peripheral blood were found to be CD71LOW/CD11a+/CD11b+/CD49d+/ CD45RA+ whereas CD34+/CLA- cells displayed the CD71+/CD11aLOW/CD11bLOW/CD49d(+)/ CD45RALOW phenotype.
	0.75	LFA-1/VLA-4 expression on CLA+/ CD34+ PBPC also allows for a more efficient binding to VCAM-1+/E-selectin+ endothelia.
19923987	0.65	PSGL-1 induce sequential intracellular signaling events in neutrophils via the Src kinase Fgr and the spleen tyrosine kinase Syk resulting in partial activation of the integrin LFA-1 with reduction in leukocyte rolling velocities.
30405637	0.64	CLA, L-selectin, CD11a, CCR4, CCR6, and CXCR4 positive (>70%).
30841639	0.58	PSGL-1, LFA-1, CD44, and VLA-4 have been described as target genes directly regulated by RUNX1/ETO.
27778308	0.52	PSGL-1 - reduced; (c) Mac-1 - reduced, unchanged, and increased; (d) LFA-1 - reduced and unchanged; (e) ICAM-1 - reduced; (f) CXCR2 - unchanged