Biomedical subjects

Ying Luo

Publications and source records attributed to Ying Luo.

36 records · Page 2Linked to original sources

PubMed2004

A photolabile hydrogel for guided three-dimensional cell growth and migration.

Tissue engineering aims to replace, repair or regenerate tissue/organ function, by delivering signalling molecules and cells on a three-dimensional (3D) biomaterials scaffold that supports cell infiltration and tissue organization. To control cell behaviour and ultimately induce structural and functional tissue formation on surfaces, planar substrates have been patterned with adhesion signals that mimic the spatial cues to guide cell attachment and function. The objective of this study is to create biochemical channels in 3D hydrogel matrices for guided axonal growth. An agarose hydrogel modified with a cysteine compound containing a sulphydryl protecting group provides a photolabile substrate that can be patterned with biochemical cues. In this transparent hydrogel we immobilized the adhesive fibronectin peptide fragment, glycine-arginine-glycine-aspartic acid-serine (GRGDS), in selected volumes of the matrix using a focused laser. We verified in vitro the guidance effects of GRGDS oligopeptide-modified channels on the 3D cell migration and neurite outgrowth. This method for immobilizing biomolecules in 3D matrices can generally be applied to any optically clear hydrogel, offering a solution to construct scaffolds with programmed spatial features for tissue engineering applications.

Animals↗

PubMed2004

The autosomal recessive polycystic kidney disease protein is localized to primary cilia, with concentration in the basal body area.

Recent evidence suggests that structural and functional abnormalities of primary cilia in kidney epithelia are associated with mouse and human autosomal dominant polycystic kidney disease. To determine whether fibrocystin/polyductin/tigmin (FPC), the protein product encoded by the PKHD1 gene that is responsible for autosomal recessive polycystic kidney disease among human subjects, is also a component of primary cilia in the kidney, antipeptide antibodies to the carboxyl-terminal intracellular domain and amino-terminal extracellular domain of FPC were generated and were characterized with immunoblotting and immuno-light and -electron microscopy. Immunolocalization in normal kidney tissue sections and cultured kidney cells demonstrated that FPC was localized to the primary cilia and concentrated on the basal bodies in both kidney tissue sections and cultured kidney cells. The FPC expression pattern was not altered in kidney cells with Pkd1 mutations. These findings suggest that FPC is a functional and/or structural component of primary cilia in kidney tubular cells. It is proposed that the pathogenesis of autosomal recessive polycystic kidney disease is linked to the dysfunction of primary cilia.

Animals↗

PubMed2004

[The analysis of different treatment methods for 184 cases of soft tissue sarcoma].

OBJECTIVE: To study the proper way of using combined postoperative chemo-radiotherapy and prognostic factors of soft tissue sarcoma. METHODS: The clinical data of 184 patients were retrospectively reviewed. These patients were devided into surgery group (S, 94 patients), surgery plus postoperative radiotherapy group (S + R, 62 patients) and surgery plus chemotherapy group (S + C, 28 patients). RESULTS: The 5-year survival rates of S, S + R and S + C groups were 39.4%, 48.4% and 28.6%, respectively. Combined multitherapy was the key to improve survival rate and life quality. Clinical stage, pathological type and therapeutic method were also important prognostic factors for the long term survival. CONCLUSION: Surgery plus postoperative radiotherapy can improve the 5-year survival rate of soft tissue sarcoma.

Adolescent↗

PubMed2004

[Cloning and expression of hTRF1 in Escherichia coli and preparation of polyclonal antibody].

Human telomeric repeat binding factor 1(TRF1) contains one Myb-type DNA-binding repeat and an amino-terminal acidic domain. It can bind to the duplex array of TTAGGG repeats at chromosome ends and is shown to be important in preserving genomic stability, maintaining cell proliferative capacity, and blocking the activation of DNA-damage cell cycle checkpoints. Interestingly, the double strand DNA breaks sensor ATM interacts with and phosphorylates Pin2/TRF1 and inhibits its function after DNA damage. Are there some proteins else that can interact with TRF1 and influence its function? In order to analysis the interaction between TRF1 and other proteins, we must prepare the antiserum that can recognize the endogenous TRF1 of cell lysates. TRF1 cDNA was amplified using cDNA Library of HeLa cell by PCR and cloned into pUCm-T vector. Sequence analysis reveals identity to the GenBank report. The TRF1 cDNA was subcloned into expression vector pET-28c(+) and expressed in E. coli as a fusion protein of 65 kD. The recombinant TRF1 can express in the supernatant (about 12.3% in total protein) on the induction of 0.5 mmol/L IPTG at 37 degrees C for 3 hours. Western-blot analysis showed the recombinant protein can react with TRF1 polyclonal antibody sc-6165 (from Santa Cruz Company). His6-TRF1 was purified by Ni(2+) -NTA resin affinity chromatography made by ourselves and showed to be homogeneity in SDS-PAGE. Rabbits were immunized for four times to prepare polyclonal antibody. The unpurified antiserum can recognize the overexpressed TRF1 with myc-tag and the endogenous Pin2/TRF1 of cell lysate by Western-blot at 1:1000 dilution. At 1:400 dilution, the antiserum can interact with endogenous TRF1 by Immunofluorescence cell staining analysis. The endogenous TRF1 in different cell lines, such as HepG2, 803, MCF7 and HeLa, locates in the nucleus. The soluble expression TRF1 and preparation of its antibody lay the foundation to study it further.

Animals↗

PubMed2004

[Effect of atorvastatin on the nuclear factor-kappaB and soluble inter-cellular adhesion molecules-1 in patients with acute coronary syndrome].

OBJECTIVE: To determine the effect of atorvastatin on the activity of peripheral blood lymocyte nuclear factor-kappaB (NF-kappaB) and plasma soluble inter-cellular adhesion molecules-1 (sICAM-1) in acute coronary syndromes. METHODS: Sixty-eight patients with acute coronary syndrome were randomly divided into atorvastatin therapeutic group (n = 37) and conventional therapeutic group (n = 31). Enzyme-linked immunosorbent assay was used to measure the plasma sICAM-1, and immunohistochemical method was used to measure the activity of NF-kappaB in the peripheral blood lymphocyte before and 12 weeks after the therapy in the two groups. RESULTS: Before the therapy, the level of NF-kappaB activity in the peripheral blood lymphocytes [(45.2 +/- 8.4)% vs (40.8 +/- 9.2)%, P > 0.05] and the plasma sICAM-1 [(357.2 +/- 84.5) ng/ml vs (365.5 +/- 91.3) ng/ml, P > 0.05] in the two groups had no significant difference. After 12 weeks of the therapy, in the conventional group the level of NF-kappaB activity in the peripheral blood lymphocytes [(40.8 +/- 9.2)% vs (38.7 +/- 8.9)%, P > 0.05] and the plasma sICAM-1 [(357.2 +/- 84.5) ng/ml vs (365.5 +/- 91.3) ng/ml, P > 0.05] still had no significant difference. But in the atorvastatin group the level of NF-kappaB activity in the peripheral blood lymphocyte [(45.2 +/- 8.4)% vs (25.6 +/- 7.9)%, P < 0.05 and the plasma soluble inter-cellular adhesion molecule-1 [(357.2 +/- 84.5) ng/ml vs (175.8 +/- 75.6) ng/ml, P < 0.05] did show a significant difference. CONCLUSION: The cholesterol-lowering therapy with atorvastatin can reduce the inflammation and stabilize the plaque in the acute coronary syndrome, which may be related to the inhibition of NF-KB and sICAM-1 activities.

Aged↗

PubMed2004

[Related inflammation markers among different types of coronary heart disease].

OBJECTIVE: To study the relationship between levels of activity of NF-kappaB p65, plasma soluble inter-cellular adhesion molecule-1, C-reactive protein on plaque stability, and different types of coronary heart disease. METHODS: We measured the levels of plasma soluble inter-cellular adhesion molecule-1 and C-reactive protein by enzyme-linked immunosorbant assay and the activity of NF-kappaB p65 in peripheral blood lymocytes immunohistochemically. RESULTS: Compared with the stable angina and the control group, the baseline activity of NF-kappaB p65, sICAM-1 and C-reactive protein was significantly elevated in the acute myocardial infarction and the unstable angina (P <0.01). After 3 month follow-up, the levels of activity of NF-kappaB p65 and sICAM-1 were unchanged (P > 0.05). In all groups, C-reactive proteins were lowered at the review (P <0.01). CONCLUSION: The levels of activity of NF-kappaB p65, sICAM-1 and C-reactive protein are related to the plaque stability among different types of coronary heart disease. NF-kappaB p65, and sICAM-1 are not affected by the acute event. These plasma markers may be important risk factors for the development of the acute coronary syndrome.

Aged↗

PubMed2003

Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells.

Several proteins implicated in the pathogenesis of polycystic kidney disease (PKD) localize to cilia. Furthermore, cilia are malformed in mice with PKD with mutations in TgN737Rpw (encoding polaris). It is not known, however, whether ciliary dysfunction occurs or is relevant to cyst formation in PKD. Here, we show that polycystin-1 (PC1) and polycystin-2 (PC2), proteins respectively encoded by Pkd1 and Pkd2, mouse orthologs of genes mutated in human autosomal dominant PKD, co-distribute in the primary cilia of kidney epithelium. Cells isolated from transgenic mice that lack functional PC1 formed cilia but did not increase Ca(2+) influx in response to physiological fluid flow. Blocking antibodies directed against PC2 similarly abolished the flow response in wild-type cells as did inhibitors of the ryanodine receptor, whereas inhibitors of G-proteins, phospholipase C and InsP(3) receptors had no effect. These data suggest that PC1 and PC2 contribute to fluid-flow sensation by the primary cilium in renal epithelium and that they both function in the same mechanotransduction pathway. Loss or dysfunction of PC1 or PC2 may therefore lead to PKD owing to the inability of cells to sense mechanical cues that normally regulate tissue morphogenesis.

Animals↗

PubMed2003

Accuracy and uniqueness of three in vivo measurements of atherosclerotic carotid plaque morphology with black blood MRI.

High-resolution MRI provides unique information about morphology of atherosclerotic carotid plaque. In this study, the accuracy and precision of measurements of carotid plaque burden and lumen narrowing were determined for in vivo black blood MRI assessment with respect to ex vivo MRI in a group of 37 atherosclerosis patients who underwent carotid endarterectomy (CEA). Three different plaque measures were compared between paired in vivo and ex vivo MR images: maximum wall area (MWA), minimum lumen area (mLA), and wall volume (WV). MWA and WV are measures of plaque burden, while mLA is a measure of lumen narrowing. The matched in vivo and ex vivo measurements showed good agreement (the correlation coefficients for in/ex vivo WV, MWA, and mLA were 0.92, 0.91, 0.90, respectively) with predictable bias. This study indicates that in vivo black blood MRI can be used to directly estimate the morphology of the plaque. Comparison of the three plaque measures showed that mLA and MWA or WV provide different information regarding the atherosclerotic lesions (the correlation coefficients between mLA and MWA or WV were less than 0.3). Black blood MRI technique is a potentially powerful clinical tool to characterize the severity of atherosclerotic plaque. It can provide accurate measurements on different aspects of the plaque, from plaque burden to lumen narrowing.

Aged↗

PubMed2003

Native polycystin 2 functions as a plasma membrane Ca2+-permeable cation channel in renal epithelia.

Mutations in polycystin 2 (PC2), a Ca(2+)-permeable cation channel, cause autosomal dominant polycystic kidney disease. Whether PC2 functions in the endoplasmic reticulum (ER) or in the plasma membrane has been controversial. Here we generated and characterized a polyclonal antibody against PC2, determined the subcellular localization of both endogenous and transfected PC2 by immunohistochemistry and biotinylation of cell surface proteins, and assessed PC2 channel properties with electrophysiology. Endogenous PC2 was found in the plasma membrane and the primary cilium of mouse inner medullar collecting duct (IMCD) cells and Madin-Darby canine kidney (MDCK) cells, whereas heterologously expressed PC2 showed a predominant ER localization. Patch-clamping of IMCD cells expressing endogenous or heterologous PC2 confirmed the presence of the channel on the plasma membrane. Treatment with chaperone-like factors facilitated the translocation of the PC2 channel to the plasma membrane from intracellular pools. The unitary conductances, channel kinetics, and other characteristics of both endogenously and heterologously expressed PC2 were similar to those described in our previous study in Xenopus laevis oocytes. These results show that PC2 functions as a plasma membrane channel in renal epithelia and suggest that PC2 contributes to Ca(2+) entry and transport of other cations in defined nephron segments in vivo.

Animals↗

PubMed2003

Measurement of carotid wall volume and maximum area with contrast-enhanced 3D MR imaging: initial observations.

PURPOSE: To investigate whether postcontrast three-dimensional (3D) magnetic resonance (MR) imaging would yield more accurate measurement of carotid artery wall volume and maximum wall area, which are both measures of plaque burden, than precontrast 3D MR imaging. MATERIALS AND METHODS: Eleven consecutive patients scheduled to undergo carotid endarterectomy were recruited for the study. A 3D fast gradient-recalled-echo sequence was applied to acquire both precontrast and postcontrast images of the carotid artery wall. The same sequence was used to image the ex vivo excised plaque as a reference for measurement of carotid wall volume and maximum wall area. RESULTS: The mean difference in maximum wall area between the precontrast in vivo measurements and the ex vivo measurements (mean +/- SD, 18.22 mm2 +/- 15.61) was significantly larger than that between the postcontrast in vivo measurements and the ex vivo measurements (12.33 mm2 +/- 14.49) (P =.02). The difference in wall volume between the precontrast in vivo measurements and the ex vivo measurements (41.81 mm3 +/- 36.51) was larger than that between the postcontrast in vivo measurements and the ex vivo measurements (32.73 mm3 +/- 35.00) (P =.004). Postcontrast images yielded better correlation with ex vivo images than did precontrast images, in both carotid luminal area (R = 0.88 for postcontrast images, R = 0.80 for precontrast images) and outer wall boundary area (R = 0.79 for postcontrast images, R = 0.71 for precontrast images) measurements. CONCLUSION: Postcontrast 3D MR imaging may be useful in the measurement of carotid artery plaque burden.

Carotid Arteries↗

PubMed2003

[Expression of osm gene driven by hTERT gene promoter inhibits cancer cells proliferation in vitro].

BACKGROUND & OBJECTIVE: Specific gene expression plays an important role in cancer gene therapy. Construction of specific expression vector is the basis of cancer gene therapy. This study was conducted to explore the expression specificity of osm (oncostatin M) gene driven by human telomerase reverse transcriptase (hTERT) gene promoter in tumor cells with telomerase activity and to investigate the growth inhibitory capability of expression of osm gene on telomerase-positive tumor cells. METHODS: The authors constructed the expression vector of osm gene afforded by the hTERT promoter and investigated its effect on tumors in vitro using reverse transcription polymerase chain reaction (RT-PCR), transient transfection, and MTT method. RESULTS: Expression of extrinsic osm gene driven by hTERT gene promoter was detected in HepG2 cell with telomerase activity, and not detected in human embryonic lung fibroblast (HEL) cell without telomerase activity. After transfection of phTERT-osm, the proliferation of HepG2, HeLa, Glc, and A549 cells showed significant inhibitory effect, and the inhibitory rate was 12.4-46%. No inhibitory effect appeared in HEL cell. CONCLUSION: The expression of osm gene under the control of hTERT gene promoter can restrict toxic effect to telomerase-positive tumor cells, and alleviate the toxic effect on normal cells without telomerase activity.

Cell Division↗

PubMed2002

ILPIP, a novel anti-apoptotic protein that enhances XIAP-mediated activation of JNK1 and protection against apoptosis.

We have previously described a new aspect of the Inhibitor of Apoptosis (IAP) family of proteins anti-apoptotic activity that involves the TAK1/JNK1 signal transduction pathway (1,2). Our findings suggest the existence of a novel mechanism that regulates the anti-apoptotic activity of IAPs that is separate from caspase inhibition but instead involves TAK1-mediated activation of JNK1. In a search for proteins involved in the XIAP/TAK1/JNK1 signaling pathway we isolated by yeast two-hybrid screening a novel X chromosome-linked IAP (XIAP)-interacting protein that we called ILPIP (hILP-Interacting Protein). Whereas ILPIP moderately activates JNK family members when expressed alone, it strongly enhances XIAP-mediated activation of JNK1, JNK2, and JNK3. The expression of a catalytically inactive mutant of TAK1 blocked XIAP/ILPIP synergistic activation of JNK1 thereby implicating TAK1 in this signaling pathway. ILPIP moderately protects against interleukin-1beta converting enzyme- or Fas-induced apoptosis and significantly potentiates the anti-apoptotic activity of XIAP. In vivo co-precipitation experiments show that both ILPIP and XIAP interact with TAK1 and tumor necrosis factor receptor-associated factor 6. Finally, expression of ILPIP did not affect the ability of XIAP to inhibit caspase activation, further supporting the idea that XIAP protection against apoptosis is achieved by two separate mechanisms: one requiring JNK1 activation and a second involving caspase inhibition.

Amino Acid Sequence↗

PubMed2002

Mutagenesis and mechanism-based inhibition of Streptococcus pyogenes Glu-tRNAGln amidotransferase implicate a serine-based glutaminase site.

The absence of Gln-tRNA synthetase in certain bacteria necessitates an alternate pathway for the production of Gln-tRNA(Gln): misacylated Glu-tRNA(Gln) is transamidated by a Gln-dependent amidotransferase (Glu-AdT) via catalysis of Gln hydrolysis, ATP hydrolysis, activation of Glu-tRNA(Gln), and aminolysis of activated tRNA by Gln-derived NH(3). As observed for other Gln-coupled amidotransferases, substrate binding, Gln hydrolysis, and transamidation by Glu-AdT are tightly coordinated [Horiuchi, K. Y., Harpel, M. R., Shen, L., Luo, Y., Rogers, K. C., and Copeland, R. A. (2001) Biochemistry 40, 6450-6457]. However, Glu-AdT does not employ an active-site Cys nucleophile for Gln hydrolysis, as is common in all other glutaminases: some Glu-AdT lack Cys, but all contain a conserved Ser (Ser176 in the A subunit of Streptococcus pyogenes Glu-AdT) within a sequence signature motif of Ser-based amidases. Our current results with S. pyogenes Glu-AdT support this characterization of Glu-AdT as a Ser-based glutaminase. Slow-onset (approximately 50 M(-1) s(-1)), tight-binding (t(1/2) > 2.5 h for complex dissociation), Gln-competitive inhibition of the Glu-tRNA(Gln)/ATP-independent glutaminase activity of Glu-AdT by gamma-Glu boronic acid is consistent with engagement of a Ser nucleophile in the glutaminase active site. Conversion to rapidly reversible, yet still potent (K(i) = 73 nM) and Gln-competitive, inhibition under full transamidation conditions mirrors the coupling between Gln hydrolysis and aminolysis reactions during productive transamidation. Site-directed replacement of Ser176 by Ala abolishes glutaminase and Gln-dependent transamidase activities of Glu-AdT (>300-fold), but retains a wild-type level of NH(3)-dependent transamidation activity. These results demonstrate the essentiality of Ser176 for Gln hydrolysis, provide additional support for coordinated coupling of Gln hydrolysis and transamidase transition states during catalysis, and validate glutaminase-directed inhibition of Glu-AdT as a route for antimicrobial chemotherapy.

Alanine↗

PubMed2002

MAPKK-independent activation of p38alpha mediated by TAB1-dependent autophosphorylation of p38alpha.

Phosphorylation of mitogen-activated protein kinases (MAPKs) on specific tyrosine and threonine sites by MAP kinase kinases (MAPKKs) is thought to be the sole activation mechanism. Here, we report an unexpected activation mechanism for p38alpha MAPK that does not involve the prototypic kinase cascade. Rather it depends on interaction of p38alpha with TAB1 [transforming growth factor-beta-activated protein kinase 1 (TAK1)-binding protein 1] leading to autophosphorylation and activation of p38alpha. We detected formation of a TRAF6-TAB1-p38alpha complex and showed stimulus-specific TAB1-dependent and TAB1-independent p38alpha activation. These findings suggest that alternative activation pathways contribute to the biological responses of p38alpha to various stimuli.

Adaptor Proteins, Signal Transducing↗

PubMed2002

Constitutive activation of G-proteins by polycystin-1 is antagonized by polycystin-2.

Polycystin-1 (PC1), a 4,303-amino acid integral membrane protein of unknown function, interacts with polycystin-2 (PC2), a 968-amino acid alpha-type channel subunit. Mutations in their respective genes cause autosomal dominant polycystic kidney disease. Using a novel heterologous expression system and Ca(2+) and K(+) channels as functional biosensors, we found that full-length PC1 functioned as a constitutive activator of G(i/o)-type but not G(q)-type G-proteins and modulated the activity of Ca(2+) and K(+) channels via the release of Gbetagamma subunits. PC1 lacking the N-terminal 1811 residues replicated the effects of full-length PC1. These effects were independent of regulators of G-protein signaling proteins and were lost in PC1 mutants lacking a putative G-protein binding site. Co-expression with full-length PC2, but not a C-terminal truncation mutant, abrogated the effects of PC1. Our data provide the first experimental evidence that full-length PC1 acts as an untraditional G-protein-coupled receptor, activity of which is physically regulated by PC2. Thus, our study strongly suggests that mutations in PC1 or PC2 that distort the polycystin complex would initiate abnormal G-protein signaling in autosomal dominant polycystic kidney disease.

GTP-Binding Proteins↗

PubMed2002

WT1 downregulation during K562 cell differentiation and apoptosis induced by bufalin.

OBJECTIVE: To study the change of WT1 gene expression during human leukemic K562 cell differentiation and apoptosis induced by bufalin. METHODS: Cell viability was determined by trypan blue exclusion, cell differentiation and apoptosis by nitro blue tetrazolium (NBT) reduction test, morphology and flow cytometry, expression of WT1 protein by Western blot analysis, and expression of WT1 mRNA by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: (1) The cell proliferation was inhibited by bufalin and the IC(50) at 24, 48, 72 h were 0.026, 0.032 and 0.006 micro mol/L, respectively. (2) Bufalin induced K562 cell differentiation towards macrophage/monocyte within concentration from 0.01 to 0.05 micro mol/L and apoptosis at higher than 0.026 micro mol/L. (3) The expression of WT1 protein and mRNA were downregulated by bufalin in the initial stage of differentiation and apoptosis induced by bufalin. CONCLUSION: K562 cell differentiation and apoptosis induced by bufalin might relate to the downregulation of WT1 expression.

Apoptosis↗

PubMed1999

Caspase-3 Gene Activity in Radiation-induced Apoptosis.

Previous experiments indicated that caspase-3 was a mediator of ionizing radiation(IR)-induced apoptosis in U937 cells. In present study the caspase-3 activity in IR-induced apoptosis was further measured by analyzing the Ac-DEVD-p-nitroanilide cleaving activity and results showed that caspase-3 activity increased in accordance to the development of apoptosis and reached peak at 6 h post-irradiation. However northern blot analysis showed that the expression of caspase-3 was not changed while Western blot found that the active P20 subunit concentration increased and from 3 h post-irradiation active P17 subunit also increased. These findings demonstrate that the increase of caspase-3 activity observed during IR-induced apoptosis depends on the activation of inactive pre-caspase rather than the change in gene expression.

Journal Article↗

PubMedDate not supplied

Light-activated immobilization of biomolecules to agarose hydrogels for controlled cellular response.

We describe a new method of synthesizing photolabile hydrogel materials for convenient photoimmobilization of biomolecules on surfaces or in 3-D matrixes. Dissolved agarose was modified with photolabile S-(2-nitrobenzyl)cysteine (S-NBC) via 1,1'-carbonyldiimidazole (CDI) activation of primary hydroxyl groups. S-NBC-modified agarose remained soluble and gelable with up to 5% S-NBC substitution, yet gelation was slower and the elastic modulus of the resulting gel was lower than those of unmodified agarose. Irradiating S-NBC-grafted agarose resulted in the loss of the protecting 2-nitrobenzyl groups, thereby exposing free sulfhydryl groups for biomolecular coupling. When appropriately activated with sulfhydryl-reactive groups, either peptides or proteins were effectively immobilized to the photoirradiated hydrogel matrixes, with the irradiation energy dose (i.e., irradiation time) used to control the amount of biomolecule immobilization. When the GRGDS peptide was immobilized on agarose, it was shown to be cell-adhesive and to promote neurite outgrowth from primary, embryonic chick dorsal root ganglion neurons. The immobilized GRGDS surface ligand concentration affected the cellular response: neurite length and density increased with GRGDS surface concentration at low adhesion ligand concentration and then plateaued at higher GRGDS concentration. Grafting 2-nitrobenzyl-protected compounds to hydrogel materials is useful for creating new photolabile hydrogel substrates for light-activated functional group generation and biomolecular immobilization.

Animals↗