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1 ialic acids and 2.4% equivalents of sulfated glycosaminoglycans).
2 ifically degrade heparan sulfate, a sulfated glycosaminoglycan.
3 nteraction is blocked by heparin, a sulfated glycosaminoglycan.
4  PF4 when it binds to CS, the major platelet glycosaminoglycan.
5 ranslational modifications apart from the CS glycosaminoglycan.
6 cable for labeling and detection of suitable glycosaminoglycans.
7 es high mannose-type N-glycans and decreases glycosaminoglycans.
8 e representatives of two major subclasses of glycosaminoglycans.
9  well to cells that are deficient in surface glycosaminoglycans.
10 s, reduced extracellular matrix proteins and glycosaminoglycans.
11 gradient is immobilized via interaction with glycosaminoglycans.
12 hat result from defects in the catabolism of glycosaminoglycans.
13 udge, focussing on sialic acids and sulfated glycosaminoglycans.
14 ediated by either elastin-binding protein or glycosaminoglycans.
15 antity and sulfation patterns of circulating glycosaminoglycans.
16 sosomal enzyme required for the breakdown of glycosaminoglycans.
17 fications observed previously on holothuroid glycosaminoglycans.
18 ncentrations of ApoB and ApoE, which bind to glycosaminoglycans.
19 to be enhanced by heparin and other sulfated glycosaminoglycans.
20 e extended to produce other isotope-enriched glycosaminoglycans.
21              Hyaluronic acid (HA) is a large glycosaminoglycan abundant in mammalian tissues that has
22           Heparan sulfate (HS) is a sulfated glycosaminoglycan abundant on the cell surface and in th
23 like structures, while staining demonstrated glycosaminoglycan accumulation.
24 s (VACV) envelope protein D8 is one of three glycosaminoglycan adhesion molecules and binds to the li
25 f AF-specific extracellular matrix (sulfated glycosaminoglycan and collagen type I), indicating a fav
26  content and orientation, water content, and glycosaminoglycan and/or proteoglycan content both in th
27                                     It binds glycosaminoglycans and certain phospholipids that can mo
28 ace glycocalyx with upregulation of sulfated glycosaminoglycans and charged glycoproteins.
29 ort that such ligands can be obscured by the glycosaminoglycans and glycoproteins that coat pathogeni
30 provide evidence that UpaB can interact with glycosaminoglycans and host fibronectin.
31 ere we show that gG attaches to cell surface glycosaminoglycans and induces lipid raft clustering, in
32 ssays that measured direct binding of Tau to glycosaminoglycans and inhibition of Tau uptake and seed
33 ptide-modified surfaces that can engage both glycosaminoglycans and integrins are effective.
34  Here, we measured vaspin binding of various glycosaminoglycans and low molecular weight heparins by
35 in many biopolymers including the polyanions glycosaminoglycans and nucleic acids.
36 ht to assess the alterations to structure of glycosaminoglycans and proteins that occur in PD brain r
37 composed of protein fibrils, hyper-sulphated glycosaminoglycans and serum amyloid P component (SAP).
38               Viral glycan receptors such as glycosaminoglycans and sialic acid-containing carbohydra
39 d infection of HCT-8 cells were inhibited by glycosaminoglycans and were reduced after heparan sulfat
40 ng, the cartilage was assayed for its water, glycosaminoglycan, and collagen content.
41 ated by treatment with trypsin or removal of glycosaminoglycans, and also suppressed by inhibition of
42  glycans, including N- and O-linked glycans, glycosaminoglycans, and carbohydrate antigens, an abilit
43 matched WT controls, including early loss of glycosaminoglycans, and decreased cartilage thickness an
44                                              Glycosaminoglycans are a group of negatively charged het
45                   Because negatively charged glycosaminoglycans are abundantly present in this layer,
46              The sulfation patterns of these glycosaminoglycans are highly variable, which presents a
47 ich applies both in vitro and in vivo, where glycosaminoglycans are strongly associated with amyloid
48 at heparan sulfate and other closely related glycosaminoglycans are the molecules that are used by fi
49 a pointed out that sialic acids and sulfated glycosaminoglycans are worth investigating in the contex
50 roteolysis at a site predicted to generate a glycosaminoglycan-bereft N-terminal fragment, versikine
51 s could potentially be attributed to reduced glycosaminoglycan binding ability, as surface plasmon re
52 nents including collagens, proteoglycans and glycosaminoglycan binding molecules.
53                   Structural analyses reveal glycosaminoglycan binding sites on Notum, which probably
54 ins: the glycoprotein, which plays a role in glycosaminoglycan binding, the fusion (F) protein, which
55 rophin (PTN) is a multifunctional, cationic, glycosaminoglycan-binding cytokine and growth factor inv
56             Evasin-3 is found to disrupt the glycosaminoglycan-binding site of CXCL8 and inhibit the
57 cluding those involved in Golgi trafficking, glycosaminoglycan biosynthesis, and glycosylphosphatidyl
58 ctional roles, including major dependency on glycosaminoglycan biosynthesis, sterol regulatory elemen
59                                 (2) GO term "glycosaminoglycan biosynthetic process" was enriched in
60                                         This glycosaminoglycan blocks the protective effect of Lys-35
61 he vasculature relies on the presentation of glycosaminoglycan-bound chemokines on the luminal side o
62                     We further validate that glycosaminoglycans but not sulfate groups are required f
63 nes are not presented to leukocytes bound to glycosaminoglycans, but rather, in solution while seques
64 nce) and a higher production of collagen and glycosaminoglycans (by histology) compared with the mono
65       Furthermore, we demonstrate that these glycosaminoglycans can block entry of and infection by f
66 ted inhibition is mainly associated with the glycosaminoglycan chains of CSPGs, and chondroitin-4-sul
67                                              Glycosaminoglycan chains of keratan sulfate proteoglycan
68  those proteins, and enzymes that can modify glycosaminoglycan chains of proteoglycans.
69             Through sulfated groups on their glycosaminoglycan chains, heparan sulfate proteoglycans
70 e show that heparan sulfate (HS), a class of glycosaminoglycan chains, regulates the number and asymm
71 h its core protein and with Ptc1 through its glycosaminoglycan chains.
72  moduli, biochemical content (i.e., sulfated glycosaminoglycans, collagen), and histological staining
73                   Hyaluronan (HA) is a major glycosaminoglycan component of the ECM and plays a signi
74                Hyaluronan is the predominant glycosaminoglycan component of the extracellular matrix
75                               It is a linear glycosaminoglycan composed of disaccharide units of GlcN
76 om differences in intracellular HA, sulfated glycosaminoglycan concentration, apoptosis, or levels of
77                         We observed abnormal glycosaminoglycan concentrations and increased concentra
78 ved from affected individuals and determined glycosaminoglycan concentrations in these cells as well
79 4.7 degrees , T2* was highly correlated with glycosaminoglycan content (r = 0.85, P < .001), the coll
80        Mature samples also exhibited greater glycosaminoglycan content and type II collagen fibre ali
81 ed cellularity, less vascularity, and higher glycosaminoglycan content when compared with control sam
82 vivo human hip cartilage correlates with the glycosaminoglycan content, equilibrium modulus, and coef
83 ing of mouse femurs was performed to measure glycosaminoglycan content, thickness, and volume of the
84                              Cellularity and glycosaminoglycans content were significantly higher in
85 age, while the ultimate strain and amount of glycosaminoglycans decreased when age increased.
86  Wnt and Hedgehog signal pathways as well as glycosaminoglycan degradation.
87 upported that roseltide rT1 enters cells via glycosaminoglycan-dependent endocytosis, and enters the
88 chondroitinase-ABC concentrations (mimicking glycosaminoglycan depletion) decreased diffusivities and
89 d ADSCs in the hydrogel, by showing enhanced glycosaminoglycan deposition and expression of chondroge
90 t catabolic stimulation for their effects on glycosaminoglycan deposition as assessed by Alcian blue
91 ds on anabolic gene expression and increased glycosaminoglycan deposition.
92  fractions of the exudate (46.7% increase in glycosaminoglycan deposition; approximately 20% upregula
93 be weakened by charge screening or enzymatic glycosaminoglycan digestion.
94             Other than their highly modified glycosaminoglycans (e.g. fucosylated chondroitin sulfate
95  we show that CD44, a major receptor for the glycosaminoglycan ECM component hyaluronan, coordinates
96 ans (eg, versican, syndecans, biglycan), and glycosaminoglycans (eg, hyaluronan, heparan sulfate) are
97                                Sulodexide, a glycosaminoglycan, exerts antithrombotic and profibrinol
98  leaflets exhibit two distinct collagen- and glycosaminoglycan-expressing interstitial cell clusters,
99 ARS-CoV-2), aminopeptidase N (for 229E), and glycosaminoglycans (for OC43).
100 llness is associated especially with altered glycosaminoglycan, GABAergic synapse, sialylation, and p
101                      A27 is one of the three glycosaminoglycan (GAG) adhesion molecules and binds to
102                          Oligomerization and glycosaminoglycan (GAG) binding of CCL5 and CCL3 are vit
103 en identified a suite of enzymes involved in glycosaminoglycan (GAG) biogenesis and transport, includ
104                                        Among glycosaminoglycan (GAG) biosynthetic enzymes, the human
105 ored in platelet alpha-granules bound to the glycosaminoglycan (GAG) chains of serglycin.
106 was to provide imaging evidence of increased glycosaminoglycan (GAG) content in patients with post-st
107                                              Glycosaminoglycan (GAG) enrichment is a dominant hallmar
108           Heparin and related members of the glycosaminoglycan (GAG) family are highly polyanionic li
109 newly identified xylose kinase essential for glycosaminoglycan (GAG) formation on the protein core of
110 r without heparan and/or chondroitin sulfate glycosaminoglycan (GAG) modifications in cells and has e
111  that it is also bound to large interstitial glycosaminoglycan (GAG) networks in different tissues, w
112                                              Glycosaminoglycan (GAG) polysaccharides have been implic
113                          Food grade sulfated glycosaminoglycan (GAG) polysaccharides were successfull
114 des as well as non-protein factors including glycosaminoglycan (GAG) polysaccharides.
115 t combining LIPUS with microbubbles enhanced glycosaminoglycan (GAG) production by 17% (5% with LIPUS
116                                              Glycosaminoglycan (GAG) sequences that selectively targe
117 ce sulfatase Sulf1 against its physiological glycosaminoglycan (GAG) target heparan sulfate (HS) by s
118                               Semi-synthetic glycosaminoglycan (GAG), generated from the sulfation of
119                     Moreover, 1B6 recognized glycosaminoglycan (GAG)-bound CXCL10, resulting in targe
120 e the promising therapeutic potential of the glycosaminoglycan (GAG)-like molecule pentosan polysulfa
121             Proteoglycans (PGs), a family of glycosaminoglycan (GAG)-protein glycoconjugates, contrib
122           It has been shown extensively that glycosaminoglycan (GAG)-protein interactions can induce,
123                                              Glycosaminoglycan (GAG)-protein interactions mediate cri
124 Degradation of the endothelial glycocalyx, a glycosaminoglycan (GAG)-rich layer lining the vascular l
125 dimers, and mediates its function by binding glycosaminoglycans (GAG) and CXCR2 receptor.
126                                              Glycosaminoglycans (GAG) are important regulators of ang
127 mple synthetic glycans, more complex natural glycosaminoglycans (GAG), and lectins/carbohydrate bindi
128     These peptides display high affinity for glycosaminoglycans (GAGs) and compete with functional in
129 E367 enhanced the viral binding affinity for glycosaminoglycans (GAGs) and reduced viremia levels and
130 his could be mediated by the xyloside-primed glycosaminoglycans (GAGs) and that these differ in compo
131                                              Glycosaminoglycans (GAGs) are a class of heterogeneous,
132 ractions between chemokines such as CCL5 and glycosaminoglycans (GAGs) are essential for creating hap
133                                              Glycosaminoglycans (GAGs) as one major part of the glyco
134                                              Glycosaminoglycans (GAGs) bind all known amyloid plaques
135 to heparin and brain-derived heparan sulfate glycosaminoglycans (GAGs) but not to the closely related
136  all-beta conformation, which interacts with glycosaminoglycans (GAGs) but not with the specific XCL1
137      Structural characterization of sulfated glycosaminoglycans (GAGs) by mass spectrometry has long
138  are mediated through the negatively charged glycosaminoglycans (GAGs) chondroitin sulfate and high-m
139                                              Glycosaminoglycans (GAGs) govern important functional ch
140                                 Cell surface glycosaminoglycans (GAGs) have been identified as CHIKV
141 es in control of mineralization, the role of glycosaminoglycans (GAGs) is less clear.
142 o susceptible host cells by interacting with glycosaminoglycans (GAGs) on the cell surface.
143                                              Glycosaminoglycans (GAGs) play vital roles in many biolo
144                                              Glycosaminoglycans (GAGs) represent a promising class of
145 (CS) proteoglycan (CSPG)-associated sulfated glycosaminoglycans (GAGs) that are selectively up-regula
146 lysine at E2 162 or 247 were more reliant on glycosaminoglycans (GAGs) to enter cells and were select
147  sulfate (DS) are l-iduronic acid containing glycosaminoglycans (GAGs) which are implicated in a numb
148  membrane-docking peptide to heparan sulfate glycosaminoglycans (GAGs) with a PTD.
149 nd and lung, we demonstrate that MCK-2 binds glycosaminoglycans (GAGs) with affinities in the followi
150                                              Glycosaminoglycans (GAGs), a category of linear, anionic
151 th the presentation of CXCL8 on cell-surface glycosaminoglycans (GAGs), an interaction that is vital
152                                              Glycosaminoglycans (GAGs), especially heparin and hepara
153 tion is intimately coupled to binding tissue glycosaminoglycans (GAGs), heparan sulfate (HS), chondro
154      Heparan sulfate belongs to the group of glycosaminoglycans (GAGs), highly sulfated linear polysa
155 n was demonstrated to interact with sulfated glycosaminoglycans (GAGs), in a Ca(2+)-independent way,
156 e of tissue-specifically expressed, sulfated glycosaminoglycans (GAGs), like HS, in determining FH bi
157                        Sema3A interacts with glycosaminoglycans (GAGs), presumably through its C-term
158 te and present CXCL12 via cell-surface-bound glycosaminoglycans (GAGs), thereby attracting CLL cells
159  Furthermore, HS, heparin, and other related glycosaminoglycans (GAGs), to different extents, can bin
160 most complex and important carbohydrates are glycosaminoglycans (GAGs), which display varied stereoch
161  or damage to elastic fibers, and pooling of glycosaminoglycans (GAGs), with associated losses of med
162 nant envelope protein of vaccinia virus, for glycosaminoglycans (GAGs)-specific targeting and imaging
163 tain non-proteinaceous components, including glycosaminoglycans (GAGs).
164 e inhibitor (serpin) family are activated by glycosaminoglycans (GAGs).
165 heir envelope glycoproteins and cell-surface glycosaminoglycans (GAGs).
166 matory processes, is known to be affected by glycosaminoglycans (GAGs).
167 t are achieved by interactions with sulfated glycosaminoglycans (GAGs).
168 se is intimately coupled to interaction with glycosaminoglycans (GAGs).
169 oteoglycans are proteins that carry sulfated glycosaminoglycans (GAGs).
170 in the IDUA gene causing the accumulation of glycosaminoglycans (GAGs).
171 ted protein 5/6 (Lrp5/6), Tetraspanin-12 and glycosaminoglycans (GAGs).
172 ), antibodies to PF4 and heparin or cellular glycosaminoglycans (GAGs).
173 ns, sialylated oligosaccharides and sulfated glycosaminoglycans (GAGs).
174 ilage matrix comprised of negatively charged glycosaminoglycans (GAGs).
175                Urine GCX breakdown products [glycosaminoglycans (GAGs)] were quantified using dimethy
176 lar matrix, consisting of negatively charged glycosaminoglycans, glycoproteins and proteoglycans in t
177 therapeutically significant glycoconjugates (glycosaminoglycans, glycoproteins, glycolipids, glycosyl
178 lasses of glycan including N- and O-glycans, glycosaminoglycans, glycosphingolipids, and glycophospha
179                    We found that the type of glycosaminoglycan has a different effect on the kinetics
180            Hyaluronan, a high molecular mass glycosaminoglycan, has been shown by us to be a suitable
181                                These complex glycosaminoglycans have important roles in cell adhesion
182 molecular species, such as glycoproteins and glycosaminoglycans, have important biological and therap
183                         Cell surface anionic glycosaminoglycans heparan sulfate and HA protect the ce
184                                          The glycosaminoglycan heparin inhibits mesangial cell growth
185                                  The natural glycosaminoglycan heparin surprisingly inhibited malaria
186 tilization hierarchy indicates that the host glycosaminoglycans heparin (Hep) and heparan sulfate (HS
187 n important constituent of the heterogeneous glycosaminoglycans heparin and heparan sulfate occurring
188 sulfate (HS) and chondroitin sulfate B (CSB) glycosaminoglycans; however, the underlying structural m
189  complex sulfation motifs of heparan sulfate glycosaminoglycans (HS GAGs) play critical roles in many
190 king the CD44 transmembrane receptor for the glycosaminoglycan hyaluronan (HA) demonstrate a number o
191                                          The glycosaminoglycan hyaluronan (HA) is a major extracellul
192 ceptor 4 (TLR4) and the extracellular matrix glycosaminoglycan hyaluronan (HA) on AEC2s are important
193  The high concentration in the stroma of the glycosaminoglycan hyaluronan, together with the large ge
194 dent on RPTPzeta and the other requiring the glycosaminoglycan hyaluronan.
195                         The breakdown of the glycosaminoglycan, hyaluronan (HA), by TMEM2 within the
196  accompanied by a coordinate loss in another glycosaminoglycan, hyaluronan.
197                        For each class of the glycosaminoglycans-hyaluronan (HA), heparan sulfate/hepa
198                  We identify the polyanionic glycosaminoglycans hyaluronic acid and heparan sulfate a
199 c acid-a high molecular extracellular matrix glycosaminoglycan implicated in playing an important rol
200 ace glycan binding proteins which facilitate glycosaminoglycan import into the periplasm; distinct ki
201 n of hyaluronan, a predominant extracellular glycosaminoglycan in developing palatal mesenchyme, play
202                 Hyaluronan (HA) is the major glycosaminoglycan in the extracellular matrix.
203 , our study uncovers a novel role of HS-type glycosaminoglycans in a local accumulation of FXIIa on t
204 l-iduronidase activity and clearing elevated glycosaminoglycans in blood and multiple organs.
205 asis is also regulated by negatively charged glycosaminoglycans in the skin interstitium, where sodiu
206  of interest, including lipids, proteins and glycosaminoglycans, in the bioengineered neo-cartilage.
207     CLEC14A physically interacted with other glycosaminoglycans, including endothelial heparan sulfat
208  to probe interactions of AgRP peptides with glycosaminoglycans, including heparan sulfate.
209 blockade of extratumoral chondroitin sulfate glycosaminoglycans inhibits glioblastoma invasion.
210 ion promotes lipoprotein deposition onto BrM glycosaminoglycans, initiating downstream effects that c
211 esults provide a more nuanced picture of PF4-glycosaminoglycan interactions leading to complex format
212      However, the current model of chemokine-glycosaminoglycan interactions, and its implications for
213 sociated with the current model of chemokine-glycosaminoglycan interactions, with implications for th
214             The structural analysis of these glycosaminoglycans is challenging due to the lability of
215 ectrometry analysis was performed to confirm glycosaminoglycan levels and sulfation patterns on donor
216         We also synthesized an orally active glycosaminoglycan (LHbisD4) that specifically binds with
217 glycolic acid (PLGA) microspheres containing glycosaminoglycan-like biopolymers (BPs), was examined.
218                           HS is a ubiquitous glycosaminoglycan located on the cell surface and tether
219 d secretion of lysosomal contents, including glycosaminoglycans, lysosomal hydrolases, and matrix met
220  of various periplasmic lyases which dictate glycosaminoglycan metabolic pathways; understanding of e
221 r study fills major gaps in our knowledge of glycosaminoglycan metabolism by the HGM.
222 ection of the genetic loci that orchestrates glycosaminoglycan metabolism in the organism Bacteroides
223 cade, lysosomes, innate immune response, and glycosaminoglycan metabolism.
224 , G protein coupled receptors, serotonin and glycosaminoglycan metabolisms among others.
225      Screening a library of 60 nonsaccharide glycosaminoglycan mimetics (NSGMs) led to the discovery
226 up of small molecules, called non-saccharide glycosaminoglycan mimetics (NSGMs), as direct allosteric
227 gical and immunological significance of this glycosaminoglycan modification and for an "ancient glyca
228 a common, but complex, malignancy-associated glycosaminoglycan modification.
229  S cleaved chemokines at the N terminus with glycosaminoglycans modulating cathepsin processing of ch
230 Both lectins bind specific sugars, including glycosaminoglycan motifs with beta1-3/beta1-4 linkages b
231 flow applicable for simultaneous analysis of glycosaminoglycans, N-glycans and proteins/peptides from
232              Hyaluronan (HA) is a ubiquitous glycosaminoglycan of the extracellular matrix.
233                Hyaluronan (HA), a ubiquitous glycosaminoglycan of the lung extracellular matrix, is r
234 Hyaluronan (HA) is one of the most prevalent glycosaminoglycans of the vascular extracellular matrix
235 ables the long-lived presentation of defined glycosaminoglycans on cell surfaces using HaloTag protei
236 sulfate (HS) and chondroitin sulfate B (CSB) glycosaminoglycans on the cell surface.
237 vivirus nonstructural protein 1 (NS1) alters glycosaminoglycans on the endothelium, causing hyperperm
238 In this study, we investigated the effect of glycosaminoglycans on the kinetics of amyloid fibril for
239  We show that T. vaginalis EVs interact with glycosaminoglycans on the surface of host cells and spec
240 s to placental dysfunction via modulation of glycosaminoglycans on trophoblasts and chorionic villi,
241 ve a variety of accessory molecules, such as glycosaminoglycans, one of the main components of the ex
242 ec-Fc was specifically inhibited by sulfated glycosaminoglycans, particularly heparin and heparan sul
243 tly by the large cross-linked assemblages of glycosaminoglycan present within leukocyte pericellular
244 ECM) is a macromolecular network composed of glycosaminoglycans, proteoglycans, glycoproteins, and fi
245                                We posit that glycosaminoglycans provide an immobilized chemokine depo
246 ontent (r = 0.85, P < .001), the collagen-to-glycosaminoglycan ratio (r = -0.79, P < .001), and water
247 hat BTV8H acquired an increased affinity for glycosaminoglycan receptors during passaging in cell cul
248 we show that a genetic point mutation in the glycosaminoglycan recognition motif of Otx2 broadly dela
249                                              Glycosaminoglycans represent an important, high priority
250                          Cartilage sulphated glycosaminoglycan (sGAG) and collagen content were asses
251 A lacking the CROPs, and identified sulfated glycosaminoglycans (sGAGs) and low-density lipoprotein r
252 employ a haploid screen to identify sulfated glycosaminoglycans (sGAGs) as its second glycan receptor
253                                    Digesting glycosaminoglycan side chains of CSPG with chondroitinas
254 se that specifically degrades the unbranched glycosaminoglycan side chains of HSPGs.
255 rting from the observation that the sulfated glycosaminoglycan-specific peptide exerts a different ef
256 creased in visceral organs of MPS-I animals, glycosaminoglycans storage was reduced, and skeletal phe
257                                        Urine glycosaminoglycan studies revealed a pathological excess
258       Pathways for the metabolism of various glycosaminoglycan substrates remain ill-defined.
259 ulfate groups of sulfated GalNAc residues of glycosaminoglycans such as chondroitin and dermatan sulf
260                                              Glycosaminoglycans such as chondroitin sulfate (CS) and
261 ry TGFbeta1 and osteogenic BMP-2, as well as glycosaminoglycans such as heparan sulfate and chondroit
262 lecular mechanisms governing interactions of glycosaminoglycans (such as heparin) with proteins remai
263  The aggregates were found to associate with glycosaminoglycans, suggesting an electrostatic mechanis
264  a carbohydrate sulfotransferase integral to glycosaminoglycan sulfation.
265 ow that biallelic mutations in EXTL3 disturb glycosaminoglycan synthesis and thus lead to a recogniza
266 gar donors were then tested as substrates in glycosaminoglycan synthesis catalyzed by various synthas
267 aran sulfate and following the inhibition of glycosaminoglycan synthesis or sulfation in HCT-8 cells.
268 ter heparan sulfate removal or inhibition of glycosaminoglycan synthesis or sulfation.
269                       Blocking sulfation and glycosaminoglycan synthesis reduces TcdA binding and ent
270 NOX4) and pathways (such as proteoglycan and glycosaminoglycan synthesis) involved in growth.
271 y decreased in CHO cell mutants defective in glycosaminoglycan synthesis.
272 A/K45A retained higher affinity for sulfated glycosaminoglycans than K42A/K110A and exhibited increas
273 ndered by the presence of hyaluronan (HA), a glycosaminoglycan that is a major fluid barrier in the i
274 ndation of extracellular matrix proteins and glycosaminoglycans that alter tumor biophysics and signa
275 abolism has been linked to the metabolism of glycosaminoglycans that are exposed on injured heart val
276 g specificity for substructures within these glycosaminoglycans that display a different degree of su
277 contains variable but often large amounts of glycosaminoglycans that influence cell and tissue functi
278  the presence of negatively charged aggrecan glycosaminoglycans that provide swelling pressures, comp
279 tructure, also enhancing the binding of this glycosaminoglycan to its cell surface receptor, CD44.
280 d thus extend the ancestry of this important glycosaminoglycan to the premetazoan era.
281  in human cells and found that RVFV utilizes glycosaminoglycans to attach to host cells.
282 red grafts, based on the quantified ratio of glycosaminoglycans to DNA and histological score, could
283 rate that FXIIa utilizes cell membrane-bound glycosaminoglycans to interact with the cell surface of
284 f murine interferon gamma (IFN-gamma), binds glycosaminoglycans to modulate serum and interstitial cy
285 ad ECs (RFPECs), including proteoglycans and glycosaminoglycans, to observe how each component indivi
286 capacity and changes in urinary excretion of glycosaminoglycans (uGAG).
287 s assayed for glycocalyx breakdown products (glycosaminoglycans) using a dimethylmethylene blue (GAG-
288 des that can be used to differentiate parent glycosaminoglycans via unsupervised multivariate analysi
289 e tool that specifically recognizes sulfated glycosaminoglycans, we analyzed the role of membrane hep
290 he biosynthesis of sialic acids and sulfated glycosaminoglycans were analyzed in the anammox draft ge
291 ins indicated that sialic acids and sulfated glycosaminoglycans were present in the anammox EPS (1.6%
292 d heparan sulfate (Hp/HS) are linear complex glycosaminoglycans which are involved in diverse biologi
293 e and heparan sulfate (HS), as well as other glycosaminoglycans, which are bioactive entities with ph
294  of filamentous proteins, proteoglycans, and glycosaminoglycans, which extensively interact and whose
295 aused a significant loss of TMJ collagen and glycosaminoglycans, which was accompanied by amplificati
296 one side of the protein for interaction with glycosaminoglycans, while the opposite face can bind fib
297  of enzymes that target substructures of the glycosaminoglycans with variable sulfation or that the g
298               Hyaluronan (HA) is an abundant glycosaminoglycan within the extracellular matrix of the
299                              Highly sulfated glycosaminoglycans within the cartilage matrix provide s
300  skin interstitium, where sodium is bound to glycosaminoglycans without commensurate effects on extra

 
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