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1 en characterizing the biological activity of inter-alpha-inhibitor.
2 ons, including the intracellular assembly of inter-alpha-inhibitor.
3 ain influence the structure and stability of inter-alpha-inhibitor.
4 both free TSG-6 (35 kd) and the complex with inter-alpha-inhibitor (120 kd) were present and upregula
5 ow TSG-6 and hyaluronan together can deplete inter-alpha-inhibitor and generate bikunin, as has been
7 ns (HCs) from the serum-derived proteoglycan inter-alpha-inhibitor are covalently attached to the HA
8 analysis shows that only the heavy chains of inter-alpha-inhibitor are incorporated into the cECM and
9 t Ca(2+), induced a conformational change in inter-alpha-inhibitor as evidenced by a decrease in the
12 n interacted with all protein components and inter-alpha-inhibitor dissociated when it was degraded.
13 of hyaluronic acid (HA) and proteins of the inter-alpha-inhibitor family plays a critical role in or
14 s serglycin, (ii) the 90-kDa core protein as inter-alpha-inhibitor heavy chain 2 (IalphaIHC2), and (i
15 lated gene 6 (TSG-6) is required to transfer inter-alpha-inhibitor heavy chains (HC) to hyaluronan (H
18 complex formed between heavy chains (HCs) of inter-alpha-inhibitor (IalphaI) and hyaluronan (HA) by t
19 nteractions of HA with hyaladherins, such as inter-alpha-inhibitor (IalphaI) and tumor necrosis facto
20 e- and dose-dependent manner and we identify Inter-alpha-inhibitor (IalphaI) as a component in serum
22 ctural similarity to bikunin, a component of inter-alpha-inhibitor (IalphaI) known for its inhibition
23 volves the transfer of heavy chains from the inter-alpha-inhibitor (IalphaI) proteoglycan, which has
24 covalent transfer of heavy chains (HCs) from inter-alpha-inhibitor (IalphaI) to hyaluronan (HA) via t
25 lently linked with the heavy chains (HCs) of inter-alpha-inhibitor (IalphaI) via a NaOH-sensitive bon
26 sential 8 (E8) formulation supplemented with inter-alpha-inhibitor (IalphaI), a human serum-derived p
27 SG-6 protein is known to form a complex with inter-alpha-inhibitor (IalphaI), a potent serine proteas
28 ains that are derived from the serum protein inter-alpha-inhibitor (IalphaI), a process that is known
30 by the cooperative action of three proteins, inter-alpha-inhibitor (IalphaI), pentraxin-3, and TNF-st
31 HA-binding proteins (hyaladherins), such as inter-alpha-inhibitor (IalphaI), versican, and tumor nec
32 ntly modified with heavy chains (HC-HA) from inter-alpha-inhibitor (IalphaI), which functions to incr
35 bitor proteins circulating in the plasma are inter-alpha-inhibitor (IalphaI, containing one light pep
38 HA after stabilization in vivo while intact inter-alpha-inhibitor is bound to the HA-enriched cECM b
39 valent interaction of HA and heavy chains of inter-alpha-inhibitor may play an important role in the
40 TSG-6-mediated transfer of heavy chains from inter-alpha-inhibitor onto HA, a process known to be ess
41 complex with the serine protease inhibitor, inter-alpha-inhibitor, potentiates the inhibition of pla
45 nostic significance of serial measurement of inter-alpha inhibitor proteins (IalphaIp) in severely se
46 recently shown that administration of human inter-alpha inhibitor proteins (IalphaIp) very early aft
50 complex with chondroitin sulfate moieties of inter-alpha-inhibitor supporting the possibility that HA
52 ctive and transfer heavy chain subunits from inter-alpha-inhibitor to either free or surface-bound hy
53 es with the heavy chain (HC) of glycoprotein inter-alpha-inhibitor to form pathological HA (HC-HA com
54 the artificial addition of heavy chains from inter-alpha-inhibitor to hyaluronan (HA), by adding reco
55 heavy chains from the chondroitin sulfate of inter-alpha-inhibitor to hyaluronan and consequently to
57 was shown to be essential for the ability of inter-alpha-inhibitor to participate in extracellular ma
59 PG were only able to accept a single HC from inter-alpha-inhibitor via transfer by TSG-6 and that HCs
60 ccepting only a single heavy chain (HC) from inter-alpha-inhibitor via transfer by tumor necrosis fac
61 that the transfer of heavy chains (HCs) from inter-alpha-inhibitor, via the enzyme TSG-6 (tumor necro
62 e interactions between hyaluronan, TSG-6 and inter-alpha-inhibitor, we recently characterized the for
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