Kamil Godula
· Associate ProfessorVerifiedUniversity of California, San Diego · Chemical and Nano Engineering
Active 2009–2026
About
Kamil Godula, Ph.D., is a Professor and Vice-Chair of Equity Diversity Inclusion and Climate in the Department of Chemistry & Biochemistry at UC San Diego. He also serves as Co-Director of the Glycobiology Research and Training Center and as Executive Secretary and Program Chair of the Division of Carbohydrate Chemistry and Chemical Glycobiology of the American Chemical Society. Born and raised in the Czech Republic, Kamil came to the United States to pursue graduate education in chemical synthesis. He received the Alfred Bader Fellowship to pursue his Ph.D. at Columbia University in the laboratory of Professor Dalibor Sames. His doctoral research focused on exploiting the unique reactivities of transition metals to streamline the construction of complex organic compounds with unique biological activities. Following his Ph.D., Kamil was an NIH K99 postdoctoral fellow in the laboratory of Professor Carolyn Bertozzi at UC Berkeley and the Molecular Foundry at the Lawrence Berkeley National Laboratory. His postdoctoral research merged synthetic chemistry, nanomaterials, and chemical biology to develop new tools for studying the interactions and functions of glycans in cancer development and metastasis. Since joining UC San Diego in 2013, his research program has focused on developing chemical methods to engineer the composition and biophysical properties of the glycocalyx of living cells. This work aims to control cellular interactions with biochemical cues, signaling pathways, and differentiation processes.
Research topics
- Cell biology
- Biochemistry
- Biology
- Virology
- Chemistry
- Internal medicine
- Computational biology
- Ecology
- Genetics
- Medicine
- Microbiology
Selected publications
Human Sulfatases Use Dual Mechanisms to Control Growth Factor–Heparan Sulfate Interactions
ACS Chemical Biology · 2026-05-18
articleSenior authorGrowth factor signaling governs essential cellular processes, and its precision relies on interactions with heparan sulfate on the cell surface. The sulfation pattern of heparan sulfate dictates its capacity to bind specific growth factors and their receptors, thereby controlling the signaling strength and specificity. Extracellular endosulfatases, including sulfatase 1 and sulfatase 2, further modulate these interactions by selectively removing sulfate groups from defined regions of heparan sulfate. Although these enzymes are known to influence developmental- and disease-related signaling, their direct effects on growth factor recognition have remained unclear. Using a panel of bioengineered heparan sulfate conjugates with defined sulfation compositions, this study examines how the structural features of heparan sulfate govern its regulation by the sulfatases. By tracking enzyme binding and catalytic remodeling, we found that both enzymes rely on two coordinated mechanisms: catalytic desulfation of heparan sulfate and competitive binding that transiently prevents growth factor association. The balance between catalytic remodeling and competitive binding depends on the sulfation characteristics of the heparan sulfate substrate and the identity of the growth factor and differs between the two enzyme isoforms. These findings provide a new framework for understanding how extracellular sulfatases shape growth factor signaling in both development and disease.
Molecular Metabolism · 2025-10-09
articleOpen accessObesity is the principal driver of insulin resistance, and lipodystrophy is also linked with insulin resistance, emphasizing the vital role of adipose tissue in glucose homeostasis. The quality of adipose tissue expansion is a critical determinant of insulin resistance predisposition, with individuals suffering from metabolic unhealthy adipose expansion exhibiting greater risk. Adipocytes are pivotal in orchestrating metabolic adjustments in response to nutrient intake and cell intrinsic factors that positively regulate these adjustments are key to prevent Type-2 diabetes. Employing unique genetic mouse models, we established the critical involvement of heparan sulfate (HS), a fundamental element of the adipocyte glycocalyx, in upholding glucose homeostasis during dietary stress. Genetic models that compromise adipocyte HS accelerate the development of high-fat diet-induced hyperglycemia and insulin resistance, independent of weight gain. Mechanistically, we show that perturbations in adipocyte HS disrupts endogenous FGF1 signaling, a key nutrient-sensitive effector. Furthermore, compromising adipocyte HS composition detrimentally impacts FGF1-FGFR1-mediated endocrinization, with no significant improvement observed in glucose homeostasis. Our data establish adipocyte HS composition as a determinant of Type 2 diabetes susceptibility and the critical dependency of the endogenous adipocyte FGF1 metabolic pathway on HS. • Adipocyte heparan sulfate does not impact diet-induced weight gain. • Adipocyte heparan sulfate sulfation compromises glucose regulation and insulin sensitivity under nutrient stress. • Mice with reduced HS sulfation show increased insulin resistance and fatty liver disease in a diet-induced obesity model. • Mechanistically HS sulfation is essential for the glucose-lowering effect of FGF1, a critical paracrine insulin sensitizer in adipose tissue.
LDL-Bound PCSK9 Has a Slower Clearance Kinetic and Higher Use for HSPGs Than Free-PCSK9—Brief Report
Arteriosclerosis Thrombosis and Vascular Biology · 2025-07-03 · 1 citations
articleOpen accessBACKGROUND: Hepatic heparan sulfate proteoglycans (HSPGs) accelerate the clearance of PCSK9 (proprotein convertase subtilisin/kexin type 9). We tested the hypothesis that free- and LDL (low-density lipoprotein)–bound PCSK9 forms have different HSPG-mediated clearance kinetics. METHODS: Metabolic and turnover studies were performed after administration of free- and LDL-bound PCSK9 to 2 HSPG knockout mouse models: (1) Global knockout of syndecan-1 ( Sdc1 −/ − ), an HSPG involved in hepatic triglyceride clearance; and (2) hepatocyte-specific knockout of heparan sulfate N-deacetylase/N-sulfotransferase (AlbCre + Ndst1 f/f ). RESULTS: The clearance of both free- and LDL-bound PCSK9 followed a 2-phase decay behavior comprising a fast and a slow phase. The more notorious effect of HSPG deletion was on the slow phase: the clearance of free-PCSK9 was faster in Sdc1 −/ − mice (t 1/2,slow [half-life on the slow phase] 13.5±1.5 minutes; P =0.0305) than in wild-type (t 1/2,slow 28.8±4.2 minutes) and AlbCre + Ndst1 f/f mice (t 1/2,slow 32.7±4.9 minutes). The clearance of LDL-bound PCSK9 was slower yet not statistically significant in Sdc1 −/ − mice (t 1/2,slow 111.2±21.6 minutes) than in wild-type (t 1/2,slow 52±6.4 minutes) and AlbCre + Ndst1 f/f mice (t 1/2,slow 39.55±2.96 minutes). However, the area under the curve showed a delayed clearance of LDL-bound PCSK9 in Sdc1 −/ − mice (44 576±2435 min×ng, P =0.004) but not in AlbCre + Ndst1 f/f (34 738±3721 min×ng, P =0.578) mice compared with wild-type (30 865±1907 min×ng). Hepatic Ndst1 -deficiency did not alter hepatic PCSK9 or LDLR (LDL receptor) expression. CONCLUSIONS: The clearance rate of plasma LDL-bound PCSK9 is slower than the clearance rate of its free form. The HSPG syndecan-1 modestly contributes to PCSK9 clearance through an LDLR-independent pathway.
Journal of the American Chemical Society · 2025-07-08 · 1 citations
articleOpen accessSenior authorCorrespondingHeparan sulfate glycosaminoglycans in the stem cell glycocalyx are crucial in controlling growth factor activity during development. Augmenting the surface of stem cells with synthetic heparan sulfate mimetics with defined compositions and growth factor binding profiles has emerged as a promising strategy to fine-tune cellular signaling responses and differentiation. However, current glycocalyx engineering methods lack specificity for stem cells or require prior genetic manipulation, limiting their applicability in a therapeutic context. Here, we report a heparan sulfate mimetic containing a DNA aptamer with affinity for the membrane-associated pluripotency marker, alkaline phosphatase, that can be selectively targeted to the surface of embryonic stem cells. The glycomimetic-enhanced fibroblast growth factor 2 recruitment to the stem cell surface activated signaling through the mitogen-activated protein kinase pathway and promoted neural differentiation. While the present work targets pluripotent cells specifically, it can be more broadly applicable to progenitor cells at other developmental stages to better control their differentiation and enhance their therapeutic potential.
Elsevier eBooks · 2025-12-05
book-chapterbioRxiv (Cold Spring Harbor Laboratory) · 2025-12-30
articleOpen accessSenior authorCorrespondingMany cancers depend on extracellular growth factors within the tumor microenvironment to drive aberrant signaling, proliferation, and survival. For example, anticancer therapies targeting vascular endothelial growth factor activity have been effective in blocking pro-angiogenic and pro-growth signals, including receptor tyrosine kinase inhibitors (e.g., Sunitinib and Sorafenib) and monoclonal antibodies (e.g., Bevacizumab). However, the effectiveness of these therapies is frequently limited by compensatory growth factor signaling and incomplete blockade, contributing to drug resistance and suboptimal long-term responses. To address these challenges, we developed Glycomimetic Lysosome-targeting Chimeras (GLYTACs) that sequester and degrade extracellular growth factors in the cancer cell environment. GLYTACs exploit growth factor interactions with cell-surface heparan sulfate (HS) glycans, a feature shared by many pro-tumorigenic signals and their receptors, by combining an HS-glycomimetic arm for growth factor binding with a polyvalent glycopolymer ligand targeting the lysosomal recycling cation-independent mannose 6-phosphate receptor (CI-M6PR) for efficient internalization and degradation. Treating HeLa cells with a heparin-based GLYTAC prototype drove rapid uptake and degradation of extracellular fibroblast growth factor 2 (FGF2). The capacity of heparin to promote the association of FGF2 with its cognate receptors (FGFRs) led to the degradation of the entire receptor-ligand complex, thereby reducing the availability of FGFRs at the cancer cell surface, which are necessary for sustained pro-oncogenic signaling. These findings highlight the potential of GLYTACs as an alternative to existing growth factor-blocking anticancer therapies and as a strategy to reshape the extracellular signaling environment of tumors.
Carbohydrates—The glycocalyx and its biological roles
Elsevier eBooks · 2025-12-05
book-chapterSenior authorAlteration of Neuropilin-1 and Heparan Sulfate Interaction Impairs Murine B16 Tumor Growth
ACS Chemical Biology · 2024-08-05 · 2 citations
articleOpen accessNeuropilin-1 acts as a coreceptor with vascular endothelial growth factor receptors to facilitate binding of its ligand, vascular endothelial growth factor. Neuropilin-1 also binds to heparan sulfate, but the functional significance of this interaction has not been established. A combinatorial library screening using heparin oligosaccharides followed by molecular dynamics simulations of a heparin tetradecasaccharide suggested a highly conserved binding site composed of amino acid residues extending across the b1 and b2 domains of murine neuropilin-1. Mutagenesis studies established the importance of arginine513 and lysine514 for binding of heparin to a recombinant form of Nrp1 composed of the a1, a2, b1, and b2 domains. Recombinant Nrp1 protein bearing R513A,K514A mutations showed a significant loss of heparin-binding, heparin-induced dimerization, and heparin-dependent thermal stabilization. Isothermal calorimetry experiments suggested a 1:2 complex of heparin tetradecasaccharide:Nrp1. To study the impact of altered heparin binding in vivo, a mutant allele of Nrp1 bearing the R513A,K514A mutations was created in mice (Nrp1D) and crossbred to Nrp1+/– mice to examine the impact of altered heparan sulfate binding. Analysis of tumor formation showed variable effects on tumor growth in Nrp1D/D mice, resulting in a frank reduction in tumor growth in Nrp1D/– mice. Expression of mutant Nrp1D protein was normal in tissues, suggesting that the reduction in tumor growth was due to the altered binding of heparin/heparan sulfate to neuropilin-1. These findings suggest that the interaction of neuropilin-1 with heparan sulfate modulates its stability and its role in tumor formation and growth.
bioRxiv (Cold Spring Harbor Laboratory) · 2023-11-22 · 1 citations
preprintOpen accessSenior authorCorrespondingAbstract Membrane-associated heparan sulfate (HS) proteoglycans (PGs) contribute to the regulation of extracellular cellular signaling cues, such as growth factors (GFs) and chemokines, essential for normal organismal functions and implicated in various pathophysiologies. PGs accomplish this by presenting high affinity binding sites for GFs and their receptors through highly sulfated regions of their HS polysaccharide chains. The composition of HS, and thus GF-binding specificity, are determined during biosynthetic assembly prior to installation at the cell surface. Two extracellular 6- O -endosulfatase enzymes (Sulf-1 and Sulf-2) can uniquely further edit mature HS and alter its interactions with GFs by removing specific sulfation motifs from their recognition sequence on HS. Despite being implicated as signaling regulators during development and in disease, the Sulfs have resisted structural characterization, and their substrate specificity and effects on GF interactions with HS are still poorly defined. Using a panel of PG-mimetics comprising compositionally-defined bioengineered recombinant HS (rHS) substrates in combination with GF binding and enzyme activity assays, we have discovered that Sulfs control GF-HS interactions through a combination of catalytic processing and competitive blocking of high affinity GF-binding sites, providing a new conceptual framework for understanding the functional impact of these enzymes in biological context. Although the contributions from each mechanism are both Sulf- and GF-dependent, the PG-mimetic platform allows for rapid analysis of these complex relationships. Significance Statement Cells rely on extracellular signals such as growth factors (GFs) to mediate critical biological functions. Membrane-associated proteins bearing negatively charged heparan sulfate (HS) sugar chains engage with GFs and present them to their receptors, which regulates their activity. Two extracellular sulfatase (Sulf) enzymes can edit HS and alter GF interactions and activity, although the precise mechanisms remain unclear. By using chemically defined HS-mimetics as probes, we have discovered that Sulfs can modulate HS by means of catalytic alterations and competitive blocking of GF-binding sites. These unique dual activities distinguish Sulfs from other enzymes and provide clues to their roles in development and disease.
Journal of Biological Chemistry · 2023-03-15 · 6 citations
articleOpen accessCorrespondingAdipose tissue plays a crucial role in maintaining metabolic homeostasis by storing lipids and glucose from circulation as intracellular fat. As peripheral tissues like adipose tissue become insulin resistant, decompensation of blood glucose levels occurs causing type 2 diabetes (T2D). Currently, modulating the glycocalyx, a layer of cell-surface glycans, is an underexplored pharmacological treatment strategy to improve glucose homeostasis in T2D patients. Here, we show a novel role for cell-surface heparan sulfate (HS) in establishing glucose uptake capacity and metabolic utilization in differentiated adipocytes. Using a combination of chemical and genetic interventions, we identified that HS modulates this metabolic phenotype by attenuating levels of Wnt signaling during adipogenesis. By engineering, the glycocalyx of pre-adipocytes with exogenous synthetic HS mimetics, we were able to enhance glucose clearance capacity after differentiation through modulation of Wnt ligand availability. These findings establish the cellular glycocalyx as a possible new target for therapeutic intervention in T2D patients by enhancing glucose clearance capacity independent of insulin secretion. Adipose tissue plays a crucial role in maintaining metabolic homeostasis by storing lipids and glucose from circulation as intracellular fat. As peripheral tissues like adipose tissue become insulin resistant, decompensation of blood glucose levels occurs causing type 2 diabetes (T2D). Currently, modulating the glycocalyx, a layer of cell-surface glycans, is an underexplored pharmacological treatment strategy to improve glucose homeostasis in T2D patients. Here, we show a novel role for cell-surface heparan sulfate (HS) in establishing glucose uptake capacity and metabolic utilization in differentiated adipocytes. Using a combination of chemical and genetic interventions, we identified that HS modulates this metabolic phenotype by attenuating levels of Wnt signaling during adipogenesis. By engineering, the glycocalyx of pre-adipocytes with exogenous synthetic HS mimetics, we were able to enhance glucose clearance capacity after differentiation through modulation of Wnt ligand availability. These findings establish the cellular glycocalyx as a possible new target for therapeutic intervention in T2D patients by enhancing glucose clearance capacity independent of insulin secretion. Type 2 diabetes (T2D) is a growing global health problem caused by excess caloric intake, reduced energy expenditure, and the resulting onset of obesity (1Palmer M.K. Toth P.P. Trends in lipids, obesity, metabolic syndrome, and diabetes mellitus in the United States: an NHANES analysis (2003-2004 to 2013-2014).Obesity (Silver Spring). 2019; 27: 309-314Crossref PubMed Scopus (79) Google Scholar, 2Unnikrishnan R. Pradeepa R. Joshi S.R. Mohan V. Type 2 diabetes: demystifying the global epidemic.Diabetes. 2017; 66: 1432-1442Crossref PubMed Scopus (206) Google Scholar). The constant nutrient influx associated with a Western diet results in high frequency of elevated blood glucose levels. This hyperglycemia demands a continuous insulin secretion from pancreatic beta cells to ensure glucose uptake for energy production and storage (3Defronzo R.A. Banting lecture. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus.Diabetes. 2009; 58: 773-795Crossref PubMed Scopus (2042) Google Scholar). The continuous insulin secretion will desensitize its perception by adipocytes, where glucose is normally stored in the form of lipids (4Olefsky J.M. Glass C.K. Macrophages, inflammation, and insulin resistance.Annu. Rev. Physiol. 2010; 72: 219-246Crossref PubMed Scopus (2057) Google Scholar, 5Rosen E.D. Spiegelman B.M. Adipocytes as regulators of energy balance and glucose homeostasis.Nature. 2006; 444: 847-853Crossref PubMed Scopus (1662) Google Scholar). This insulin resistance coincides with the onset of T2D, leading ultimately to beta cell failure (6Halban P.A. Polonsky K.S. Bowden D.W. Hawkins M.A. Ling C. Mather K.J. et al.beta-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment.Diabetes Care. 2014; 37: 1751-1758Crossref PubMed Scopus (333) Google Scholar, 7Lee Y.S. Olefsky J. Chronic tissue inflammation and metabolic disease.Genes Dev. 2021; 35: 307-328Crossref PubMed Google Scholar). T2D patients have a high risk to develop neuropathy, retinopathy, cardiovascular disease, stroke, and poor outcomes when coping with infectious disease (8Drucker D.J. Diabetes, obesity, metabolism, and SARS-CoV-2 infection: the end of the beginning.Cell Metab. 2021; 33: 479-498Abstract Full Text Full Text PDF PubMed Scopus (141) Google Scholar). Overall, this greatly reduces their quality of life and life expectancy. As a result, T2D has been a prominent focus of medical research to find effective treatments. Current treatment strategies focused on increasing insulin perception, augmenting oxidative tissue activity, or decreasing excessive food consumption or nutrient absorption have been limited by poor efficacy or detrimental side-effects as exemplified by the COVID-19 pandemic (8Drucker D.J. Diabetes, obesity, metabolism, and SARS-CoV-2 infection: the end of the beginning.Cell Metab. 2021; 33: 479-498Abstract Full Text Full Text PDF PubMed Scopus (141) Google Scholar, 9Pasquel F.J. Lansang M.C. Dhatariya K. Umpierrez G.E. Management of diabetes and hyperglycaemia in the hospital.Lancet Diabetes Endocrinol. 2021; 9: 174-188Abstract Full Text Full Text PDF PubMed Scopus (92) Google Scholar, 10Lim S. Bae J.H. Kwon H.S. Nauck M.A. COVID-19 and diabetes mellitus: from pathophysiology to clinical management.Nat. Rev. Endocrinol. 2021; 17: 11-30Crossref PubMed Scopus (509) Google Scholar). An alternative approach to increase insulin-independent glucose clearance is to capitalize on adipose tissue expandability and its functional metabolic flexibility and reprogram adipogenesis to increase basal glucose clearance capacity in adipose tissue (11Christodoulides C. Lagathu C. Sethi J.K. Vidal-Puig A. Adipogenesis and WNT signalling.Trends Endocrinol. Metab. 2009; 20: 16-24Abstract Full Text Full Text PDF PubMed Scopus (455) Google Scholar, 12Scherer P.E. The many secret lives of adipocytes: implications for diabetes.Diabetologia. 2019; 62: 223-232Crossref PubMed Scopus (100) Google Scholar, 13Scherer P.E. The multifaceted roles of adipose tissue-therapeutic targets for diabetes and beyond: the 2015 banting lecture.Diabetes. 2016; 65: 1452-1461Crossref PubMed Scopus (90) Google Scholar, 14Carobbio S. Pellegrinelli V. Vidal-Puig A. Adipose tissue function and expandability as determinants of lipotoxicity and the metabolic syndrome.Adv. Exp. Med. Biol. 2017; 960: 161-196Crossref PubMed Scopus (123) Google Scholar). The cellular glycocalyx has been well-established to play a regulatory role during adipogenesis and in adipocyte function and can serve as a potential target for therapeutic intervention in T2D (15Pessentheiner A.R. Ducasa G.M. Gordts P. Proteoglycans in obesity-associated metabolic dysfunction and meta-inflammation.Front. Immunol. 2020; 11: 769Crossref PubMed Scopus (42) Google Scholar, 16Dokoshi T. Zhang L.J. Nakatsuji T. Adase C.A. Sanford J.A. Paladini R.D. et al.Hyaluronidase inhibits reactive adipogenesis and inflammation of colon and skin.JCI Insight. 2018; 3Crossref PubMed Scopus (25) Google Scholar, 17Zhu Y. Kruglikov I.L. Akgul Y. Scherer P.E. Hyaluronan in adipogenesis, adipose tissue physiology and systemic metabolism.Matrix Biol. 2019; 78-79: 284-291Crossref PubMed Scopus (32) Google Scholar). Although, the functions of specific cell-surface glycans during adipogenic programing and their impact on glucose clearance capacity of terminally differentiated adipocytes are yet to be fully elucidated. For instance, an unbiased proteomic screen of human adipose tissues and plasma identified glypican 4 (GPC4), a heparan sulfate (HS) proteoglycan, as an adipokine (15Pessentheiner A.R. Ducasa G.M. Gordts P. Proteoglycans in obesity-associated metabolic dysfunction and meta-inflammation.Front. Immunol. 2020; 11: 769Crossref PubMed Scopus (42) Google Scholar, 18Gesta S. Bluher M. Yamamoto Y. Norris A.W. Berndt J. Kralisch S. et al.Evidence for a role of developmental genes in the origin of obesity and body fat distribution.Proc. Natl. Acad. Sci. U. S. A. 2006; 103: 6676-6681Crossref PubMed Scopus (474) Google Scholar). plasma levels with the of insulin glucose and high body (15Pessentheiner A.R. Ducasa G.M. Gordts P. Proteoglycans in obesity-associated metabolic dysfunction and meta-inflammation.Front. Immunol. 2020; 11: 769Crossref PubMed Scopus (42) Google Scholar, S. Bluher M. insulin signaling with the insulin and as a novel PubMed Scopus Google Scholar). or of is associated with an in adipogenesis in in of glucose insulin and in adipocytes S. Bluher M. insulin signaling with the insulin and as a novel PubMed Scopus Google Scholar). is the adipokine function of from the or its with HS glycans M. K. S. A. K. of heparan sulfate differentiation potential of Biol. Full Text Full Text PDF PubMed Scopus Google Scholar). HS are of of and are through the and (15Pessentheiner A.R. Ducasa G.M. Gordts P. Proteoglycans in obesity-associated metabolic dysfunction and meta-inflammation.Front. Immunol. 2020; 11: 769Crossref PubMed Scopus (42) Google Scholar). These with are by heparan Rev. 2014; PubMed Scopus Google Scholar). HS has been in the of uptake and P. The heparan sulfate on and Biol. 2018; PubMed Scopus Google Scholar). in in differentiated adipocytes an HS proteoglycan, or the HS have been to of J.M. A. et heparan sulfate clearance of of PubMed Scopus Google Scholar, et is the heparan sulfate clearance of in 2009; Google Scholar). of the regulatory roles of HS in cellular signaling and differentiation S. sulfate Biol. 3Crossref PubMed Scopus Google we to the possible roles of HS during adipogenic differentiation in the metabolic of terminally differentiated adipocytes. 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Metab. 2009; 20: 16-24Abstract Full Text Full Text PDF PubMed Scopus (455) Google Scholar, heparan Rev. 2014; PubMed Scopus Google Scholar, S. sulfate Biol. 3Crossref PubMed Scopus Google Scholar). The genes by HS in the of adipogenesis are Wnt genes and of the Wnt with Wnt the genes and were in HS cells to These are with the role for Wnt signaling in adipocyte during adipogenesis (11Christodoulides C. Lagathu C. Sethi J.K. Vidal-Puig A. Adipogenesis and WNT signalling.Trends Endocrinol. Metab. 2009; 20: 16-24Abstract Full Text Full Text PDF PubMed Scopus (455) Google Scholar). HS Wnt in this is and K. R. Wnt Biol. PubMed Scopus Google Scholar, Y. S. sulfate in Wnt signaling and Dev. Biol. 2020; PubMed Scopus Google Scholar). that the functional role of HS is to Wnt during adipogenesis S. sulfate Biol. 3Crossref PubMed Scopus Google Scholar, M. U. the of cell heparan sulfate to Wnt Biol. PubMed Scopus Google Scholar, M. S. K. screen heparan sulfate WNT and PubMed Scopus Google Scholar). this we differentiation in and in the or of of the Wnt signaling and as as inhibits the of the signaling Wnt the glucose uptake capacity in adipocytes and and and a in cells and These that of Wnt signaling during of adipogenesis in cells glucose uptake in adipocytes after results to the role of cell HS in Wnt activity, by the ligand from its Y. S. sulfate in Wnt signaling and Dev. Biol. 2020; PubMed Scopus Google Scholar). the Wnt signaling has been as a therapeutic for increasing glucose uptake capacity in adipose tissues (11Christodoulides C. Lagathu C. Sethi J.K. Vidal-Puig A. Adipogenesis and WNT signalling.Trends Endocrinol. Metab. 2009; 20: 16-24Abstract Full Text Full Text PDF PubMed Scopus (455) Google Scholar, R. the Dev. Biol. 2021; PubMed Scopus Google Scholar). in we were able to to increase in glucose in cells in the of chemical Wnt signaling the an alternative strategy to the capacity of the glycocalyx to Wnt signaling in to enhance glucose the cell of and to synthetic of HS D.J. K. glycocalyx for in Sci. 2021; 9: PubMed Google Scholar). 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Management of diabetes and hyperglycaemia in the hospital.Lancet Diabetes Endocrinol. 2021; 9: 174-188Abstract Full Text Full Text PDF PubMed Scopus (92) Google Scholar). An alternative approach of fat tissues to increase their cellular and glucose (11Christodoulides C. Lagathu C. Sethi J.K. Vidal-Puig A. Adipogenesis and WNT signalling.Trends Endocrinol. Metab. 2009; 20: 16-24Abstract Full Text Full Text PDF PubMed Scopus (455) Google Scholar, 12Scherer P.E. The many secret lives of adipocytes: implications for diabetes.Diabetologia. 2019; 62: 223-232Crossref PubMed Scopus (100) Google Scholar, 13Scherer P.E. The multifaceted roles of adipose tissue-therapeutic targets for diabetes and beyond: the 2015 banting lecture.Diabetes. 2016; 65: 1452-1461Crossref PubMed Scopus (90) Google Scholar, 14Carobbio S. Pellegrinelli V. Vidal-Puig A. Adipose tissue function and expandability as determinants of lipotoxicity and the metabolic syndrome.Adv. Exp. Med. Biol. 2017; 960: 161-196Crossref PubMed Scopus (123) Google Scholar). 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Lagathu C. Sethi J.K. Vidal-Puig A. Adipogenesis and WNT signalling.Trends Endocrinol. Metab. 2009; 20: 16-24Abstract Full Text Full Text PDF PubMed Scopus (455) Google Scholar, S. sulfate Biol. 3Crossref PubMed Scopus Google Scholar, K. R. Wnt Biol. PubMed Scopus Google Scholar, R. the Dev. Biol. 2021; PubMed Scopus Google Scholar). Wnt is to its in as as of HS function during adipogenesis R. the Dev. Biol. 2021; PubMed Scopus Google Scholar). HS can and cell signaling signaling or by from P. The heparan sulfate on and Biol. 2018; PubMed Scopus Google Scholar, S. sulfate Biol. 3Crossref PubMed Scopus Google Scholar). this we that cell HS pre-adipocytes to Wnt to an role of cell HS in Wnt This by the of the of of Wnt identified that the of a of and can the of as a ligand to T. K. 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Recent grants
NIH · $485k · 2016
UCSD Biomedical Scientist Career Development Program in Glycoscience
NIH · $5.3M · 2018–2024
Glycan array for phenotype-driven capture and genotyping of viruses in primary isolates
NIH · $601k · 2016–2019
NIH · $2.3M · 2020
NIH · $238k · 2016
Frequent coauthors
- 36 shared
Carolyn R. Bertozzi
Stanford University
- 17 shared
Mia L. Huang
Torrey Pines Institute For Molecular Studies
- 12 shared
David Rabuka
- 12 shared
Philip L.S.M. Gordts
University of California, San Diego
- 10 shared
Greg W. Trieger
University of California, San Diego
- 10 shared
Thomas Mandel Clausen
University of California, San Diego
- 10 shared
Logan K. Laubach
Virginia Commonwealth University
- 9 shared
R. Parthasarathy
University of Oregon
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