Publication for Anxa5 and Anxa2

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Anxa5	annexin A5	11747			[link]
mmu	Anxa2	annexin A2	12306

Pubmed ID	Priority	Text
25222280	0.98	AnxA2 and AnxA5 knockdown cells.
	0.98	AnxA2 and AnxA5 can influence bone formation via regulation of osteoprogenitor proliferation, differentiation, and responsiveness to cytokines in addition to their well-studied function in matrix vesicles.
	0.98	AnxA2 and AnxA5 are present in matrix vesicles secreted by hypertrophic chondrocytes and osteoblasts.
	0.98	AnxA2kd and AnxA5kd each demonstrated decreased responsiveness to the anti-inflammatory cytokine interleukin 4 (IL-4), indicating that both AnxA2 and AnxA5 are required for maximal responsiveness.
	0.98	AnxA2kd and AnxA5kd cells compared to Si controls ( Figure 3C ), suggesting that the ordered process of osteogenic differentiation was subtly altered in AnxA2kd and AnxA5kd cells.
	0.98	AnxA2kd nor AnxA5kd cells demonstrated significant increases in luciferase activity in response to IL-4, indicating that reduced AnxA2 or AnxA5 expression compromises STAT6 signaling.
	0.98	AnxA2 and AnxA5 are present in matrix vesicles isolated from both chondrocytes and osteoblasts, where they are thought to act as membrane channels to allow Ca2+ influx and hydroxyapatite crystal formation.
	0.98	AnxA2 and AnxA5 at similar levels, as determined by both mRNA and protein ( Figure 1A-C ).
	0.98	AnxA2 or AnxA5 reductions upon osteogenic differentiation either is Runx2-independent or involves processes initiated after induction of Runx2.
	0.98	AnxA2kd and AnxA5kd cultures compared to Si, wherein its expression was significantly lower in either knockdown cell type at 21 days of culture ( Figure 3B ); these suggest that both AnxA2 and AnxA5 are required for maximal induction of Sp7 expression under the course of osteogenic differentiation.
	0.98	AnxA2 and AnxA5 are each dynamically expressed during the course of osteogenic differentiation.
	0.98	AnxA2 or AnxA5 decreased DNA content to the same degree ( Figure 2A-C ), there exist subtle differences in the effect of AnxA2 or AnxA5 knockdown upon osteoprogenitor differentiation.
	0.98	AnxA2kd or AnxA5kd cells compared to Si controls ( Figure 6 ).
	0.98	AnxA2kd and AnxA5kd cells, it is possible that AnxA2 and AnxA5 function as regulators of transcription in osteoblastic cells.
	0.98	AnxA2 and AnxA5 are involved in pre-osteoblast proliferation, the timing and magnitude of osteogenic gene expression, matrix maturation, and responsiveness to anti-inflammatory cytokines.
	0.97	AnxA2- and AnxA5-knockdown, interleukin-induced STAT6 signaling was markedly attenuated compared to pSiren controls.
	0.97	AnxA2 or AnxA5 decreased proliferation and altered the dynamic course of osteogenic differentiation compared to pSiren (Si) control cells.
	0.97	AnxA2, and AnxA5, have cell-autonomous roles during multiple stages of osteogenic differentiation-proliferation, matrix formation and organization, and matrix mineralization.
	0.97	AnxA2kd and AnxA5kd cells have decreased proliferative capacity compared to Si cells ( Figures 2A-C ), and suppression of AnxA2 by shRNA similarly decreases proliferation of adenocarcinoma, breast cancer, and multiple myeloma cells.
	0.97	AnxA2 and AnxA5 may be required for the ordered, sequential processes inherent in osteoblast differentiation.
	0.97	AnxA2 or AnxA5 expression and osteogenesis, which is confirmed by our differentiation studies in AnxA2kd and AnxA5kd cells.
	0.97	AnxA2 or AnxA5 functioning as ion channels to regulate cytosolic calcium levels, critical determinants of progression through the cell cycle and gene transcription.
	0.96	AnxA2 in matrix mineralization, whether either AnxA2 or AnxA5 have cell-autonomous effects on processes occurring prior to mineralization-proliferation and osteogenic differentiation-remains unexamined.
	0.96	AnxA2 and AnxA5 in proliferation of pre-osteoblasts, matrix maturation and mineralization.
	0.96	AnxA2 and AnxA5 knockdown on expression of genes associated with osteogenic differentiation.
	0.96	AnxA2 and AnxA5 expression increased as a function of time when cells were cultured in osteogenic media, with AnxA2 demonstrating significantly increased expression at d14 and d21, and AnxA5 revealing maximal expression at d14 but then returning toward baseline at d21.
	0.96	AnxA2kd and AnxA5kd cells was disrupted compared to Si controls.
	0.96	AnxA2 and AnxA5 likely exert non-redundant roles in osteogenesis.
	0.95	AnxA2 or AnxA5 exert cell-autonomous roles in an osteoblast.
	0.95	AnxA2 and AnxA5 expression as a function of time in culture under osteogenic differentiation-inducing conditions are dynamic.
	0.94	AnxA5kd cells similarly demonstrated less staining compared to Si controls, although staining was more pronounced in AnxA5kd compared to AnxA2kd at both days 14 and 21, indicating that AnxA5kd cells have an osteogenic potential that is intermediate between Si controls and AnxA2kd cells.
	0.94	AnxA2 or AnxA5 attenuate pre-osteoblast proliferation and alter the timing of osteogenic differentiation, we began to examine mechanistic explanations for the observed results.
	0.93	AnxA2 and AnxA5 are dynamically-expressed during osteogenic differentiation
	0.93	AnxA2 and AnxA5 are maximally expressed.
	0.92	AnxA2 and AnxA5 in osteogenesis.
	0.91	AnxA2kd and AnxA5kd cells ( Figure 3A ), although Sp7 expression decreased significantly at 21 days in culture compared to Si controls ( Figure 3B ).
	0.91	AnxA2 and AnxA5 expression increased significantly after 14 days in culture ( Figures 5A and 5B ); AnxA2 remained elevated, whereas AnxA5 returned to baseline, at 21 days.
	0.91	AnxA2kd cells compared to AnxA5kd, which themselves showed no difference compared to Si ( Figure 4C ).
	0.88	AnxA2 mRNA expression in AnxA2kd cells compared to Si-transfected controls ( Figure 1A ), and there was no compensatory change in AnxA5 mRNA in AnxA2kd cells.
	0.88	AnxA2kd (14% reduction) and in AnxA5kd (20% reduction) cells, relative to Si control ( Figure 2A ).
	0.88	AnxA2kd and AnxA5kd cells compared to Si controls after 14 days in culture ( Figure 3E ).
	0.86	AnxA2 or AnxA5 attenuate IL-4-induced signaling
	0.85	AnxA2 and AnxA5 mRNA and protein, we next examined whether alterations in AnxA2 or AnxA5 expression influenced pre-osteoblast proliferation.
	0.85	AnxA2kd cells compared to AnxA5kd cells.
	0.82	AnxA2 or AnxA5 (AnxA2kd and AnxA5kd, respectively) upon the proliferation and osteogenic differentiation of the pre-osteoblast MC3T3-E1 cell line.
	0.77	AnxA5 mRNA in AnxA5kd cells compared to Si control, and no effect of AnxA5 depletion upon AnxA2 mRNA expression ( Figure 1B ).
	0.77	AnxA2kd and AnxA5kd cells.
	0.75	AnxA2- or AnxA5-knockdown after 14 days of culture.
	0.63	AnxA2 and AnxA5.
	0.59	AnxA2 or AnxA5 reduction upon markers of osteogenic differentiation.
10973999	0.98	Annexin II promotes the Ca2+-dependent association of lipid raft microdomains, whereas annexin V interacts with glycerophospholipid microcompartments.
	0.97	annexin V binding to biological membranes, annexin II exhibits a preference for different lipid moieties.
	0.97	Annexin II and annexin V interact with different membrane lipid microcompartments.
	0.82	annexin II (Fig. 5 d) pelleted with the raft markers, cholesterol, sphingomyelin (Fig. 5 c), and 5'-nucleotidase (Fig. 5 b), whereas annexin V was gradually extracted by the detergent (Fig. 5 d) after the removal of glycerophospholipids (Fig. 5 c).
25597631	0.98	annexin A2, but not annexin A5, in Atg16L-positive vesicles, and confirmed the role of Ca2+ in recruitment of annexin A2 from the cytosol (Fig. 1g, Supplementary Fig. 1).
26182056	0.98	Anxa5 being present in mouse embryonic blood vessels (Fig 3E and 3F), we found that Anxa2 and Anxa6 are expressed in the early embryonic endothelium of mice (S5A and S5B Fig).
21468022	0.97	AnxA5 forms heterogenous assemblies with AnxA1 or AnxA2 on plasma membranes of ionomycin-treated cells and speculated that such assemblies participate in membrane repair.
	0.97	AnxA2 (ref.) and AnxA5 (ref.), respectively, can indeed be understood in the context of a global machinery protecting cells against damages resulting from membrane rupture.
	0.96	AnxA2 and AnxA5, which possess anti-inflammatory, pro-fibrinolytic and anti-thrombotic activities, respectively.
25976293	0.97	Annexin A2, which is expressed in mouse primary sensory neurons, causes neuropathic pain, while Annexin 5 possesses a role in the pathogenesis of autoimmune sensory neuropathy in humans.
26793286	0.96	AnxA2, AnxA4, AnxA5 and AnxA6 and agree with pathophysiological disturbances in Ca2 +-buffering and membrane organization.
27251877	0.94	ANXA5 was also the most abundant annexin in whole utricle, ANXA2 and ANXA6 were present at substantial levels (Fig. 1a).
	0.93	ANXA5 is likely to be in the hair-cell soma, not bundle, and the other annexins (ANXA2 and ANXA6) highly expressed in the soma may be capable of taking the place of ANXA5.
	0.84	ANXA2 and ANXA6 also bind to anionic phospholipids in the presence of Ca2+, binding affinities and lipid specificities vary and so ANXA5 may bind more avidly to stereocilia binding sites.
	0.80	ANXA2, ANXA4, and ANXA6, but they were all far less abundant than ANXA5 and none of them changed significantly in Anxa5-/- bundles.
26324419	0.94	Anxa2, Anxa4, Anxa5).
28951044	0.94	ANXA5 in DC lenses, whereas ANXA2 and ANXA5 were upregulated in GSH-deficient lenses (Appendix 2).
20170493	0.87	Anxa2 and Anxa5, encode members of the annexin family.
30254199	0.74	Anxa2, Anxa5, or Anxa6 have been generated and used to evaluate the physiological roles of Annexins.