Professor, Medicine, University of Washington School of Medicine

Internal Medicine

Stuart J. Shankland is an expert in the field of Internal Medicine. Stuart J. Shankland, MD is a published doctor as well. He has 99 publications published. The latest was: The growing role for the cyclin kinase inhibitor p27Kip1 in renal disease. He accepts all Medicare patients.

Publications

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• Dicer1 activity in the stromal compartment regulates nephron differentiation and vascular patterning during mammalian Kidney organogenesis.
• Deficient Autophagy Results in Mitochondrial Dysfunction and FSGS.
• The Pathogenesis of Focal Segmental Glomerulosclerosis.
• Cells of renin lineage take on a podocyte phenotype in aging Nephropathy.
• Cells of Renin Lineage Are Progenitors of Podocytes and Parietal Epithelial Cells in Experimental Glomerular Disease.
• Has the circulating permeability factor in primary FSGS been found?
• Reversibility of structural and functional damage in a model of advanced diabetic Nephropathy.
• Glomerular parietal epithelial cells in Kidney physiology, pathology, and repair.
• Podocyte Repopulation by Renal Progenitor Cells Following Glucocorticoids Treatment in Experimental FSGS.
• Both cyclin I and p35 are required for maximal survival benefit of Cyclin-dependent kinase 5 in Kidney podocytes.
• SSeCKS sequesters cyclin D1 in glomerular parietal epithelial cells and influences proliferative injury in the glomerulus.
• De novo expression of podocyte proteins in parietal epithelial cells in experimental aging Nephropathy.
• Mannose Receptor 2 Attenuates Renal Fibrosis.
• Albumin-induced apoptosis of glomerular parietal epithelial cells is modulated by extracellular signal-regulated kinase 1/2.
• Podocyte Disorders: Core Curriculum 2011.
• Podocyte Biology for the Bedside.
• Role of smooth muscle protein SM22{alpha} in glomerular epithelial cell injury.
• Dystroglycan does not contribute significantly to Kidney development or function, in health or after injury.
• A suPAR circulating factor causes Kidney disease.
• BTBR Ob/Ob mutant mice model progressive diabetic Nephropathy.
• Cyclin I-Cdk5 governs survival in post-mitotic cells.
• p35, the non-cyclin activator of Cdk5, protects podocytes against apoptosis in vitro and in vivo.
• De novo expression of podocyte proteins in parietal epithelial cells during experimental glomerular Disease.
• The CDK-inhibitor p21 is Pro-survival in Adriamycin(R)-Induced Podocyte Injury, in vitro and in vivo.
• Novel siRNA delivery system to target podocytes in vivo.
• Experimental Models of Membranous Nephropathy.
• A new function for parietal epithelial cells: a second glomerular barrier.
• The enigmatic parietal epithelial cell is finally getting noticed: a review.
• Cyclin I activates Cdk5 and regulates expression of Bcl-2 and Bcl-XL in postmitotic mouse cells.
• Creating research infrastructure and functionality to address chronic Kidney disease: the Kidney Research Institute.
• Focal and segmental glomerulosclerosis induced in mice lacking decay-accelerating factor in T cells.
• Inducible rodent models of acquired podocyte Diseases.
• Establishment of conditionally immortalized mouse glomerular parietal epithelial cells in culture.
• Activation of a local renin angiotensin system in podocytes by glucose.
• TLR4 links podocytes With the innate immune system to mediate glomerular injury.
• Protease nexin-1, tPA, and PAI-1 are upregulated in cryoglobulinemic membranoproliferative glomeruloNephritis.
• Induction of TRPC6 channel in acquired forms of proteinuric Kidney disease.
• Cyclin I protects podocytes from apoptosis.
• Giant cell tubulitis With tubular basement membrane immune deposits: a report of two cases after cardiac valve replacement surgery.
• Glial cell line-derived neurotrophic factor and its receptor ret is a novel ligand-receptor complex critical for survival Response during podocyte injury.
• The renin-angiotensin system in glomerular podocytes: mediator of glomerulosclerosis and link to Hypertensive nephropathy.
• Protection of endothelial cells by dextran sulfate in rats With thrombotic microangiopathy.
• p27(Kip1) Knockout mice are protected from diabetic Nephropathy: evidence for p27(Kip1) haplotype insufficiency.
• The cyclin-dependent kinase inhibitor p21 is required for TGF-beta1-induced podocyte apoptosis.
• Dexamethasone prevents podocyte apoptosis induced by puromycin aminonucleoside: role of p53 and Bcl-2-related family proteins.
• Mechanical strain increases SPARC levels in podocytes: implications for glomerulosclerosis.
• ATRA induces podocyte differentiation and alters nephrin and podocin expression in vitro and in vivo.
• Urinary podocyte loss is a more specific marker of ongoing glomerular damage than Proteinuria.
• Cellular Response to injury in membranous nephropathy.
• Limitation of podocyte proliferation improves Renal function in experimental crescentic glomerulonephritis.
• Mechanical stretch induces podocyte hypertrophy in vitro.
• Cyclin-dependent kinase 5 is a regulator of podocyte differentiation, proliferation, and morphology.
• The rapamycin derivative RAD inhibits mesangial cell migration through the CDK-inhibitor p27KIP1.
• Negatively regulating the cell cycle can be positive.
• Differential expression of d-type cyclins in podocytes in vitro and in vivo.
• Not just an inhibitor: a role for p21 beyond the cell cycle-"The truth is rarely pure and never simple".
• Activation of a local tissue angiotensin system in podocytes by mechanical strain.
• The role of cell cycle proteins in Glomerular Disease.
• Podocytes that detach in experimental membranous Nephropathy are viable.
• Angiotensin II-induced hypertrophy of proximal tubular cells requires p27Kip1.
• Hematopoietic stem cells contribute to the regeneration of Renal tubules after Renal ischemia-reperfusion injury in mice.
• P27Kip1: the "rosebud" of diabetic Nephropathy?
• DNA damage is a novel Response to sublytic complement C5b-9-induced injury in podocytes.
• Mitotic cell cycle proteins increase in podocytes despite lack of proliferation.
• Models of glomeruloNephritis.
• Podocyte biology and Response to injury.
• Effects of cyclosporine in osteopontin null mice.
• The hypertrophic effect of transforming growth factor-beta is reduced in the absence of cyclin-dependent kinase-inhibitors p21 and p27.
• Insulin is a potent survival factor in mesangial cells: role of the PI3-kinase/Akt pathway.
• Cyclooxygenase-2 overexpression inhibits platelet-derived growth factor-induced mesangial cell proliferation through induction of the tumor suppressor gene p53 and the...
• Mechanical stress reduces podocyte proliferation in vitro.
• Podocyte expression of the CDK-inhibitor p57 during development and Disease.
• High glucose-induced hypertrophy of mesangial cells requires p27(Kip1), an inhibitor of cyclin-dependent kinases.
• Complement (C5b-9) induces DNA synthesis in rat mesangial cells in vitro.
• Vascular endothelial growth factor accelerates Renal recovery in experimental thrombotic microangiopathy.
• Differential expression of cyclin-dependent kinase inhibitors in human glomerular Disease: role in podocyte proliferation and maturation.
• C5b-9 membrane attack complex mediates endothelial cell apoptosis in experimental glomeruloNephritis.
• Cell cycle regulatory proteins in Renal disease: role in hypertrophy, proliferation, and apoptosis.
• New insights into the pathogenesis of membranous Nephropathy.
• Cell cycle regulatory proteins in glomerular Disease.
• Cyclin kinase inhibitor p21CIP1/WAF1 limits interstitial cell proliferation following ureteric obstruction.
• The cyclin kinase inhibitor p21WAF1/CIP1 is required for glomerular hypertrophy in experimental diabetic Nephropathy.
• Obstructive uropathy in the mouse: role of osteopontin in interstitial fibrosis and apoptosis.
• Complement (C5b-9) induces glomerular epithelial cell DNA synthesis but not proliferation in vitro.
• The cyclin kinase inhibitor p21CIP1/WAF1 limits glomerular epithelial cell proliferation in experimental glomeruloNephritis.
• Glomerular podocytes and adhesive interaction With glomerular basement membrane.
• Modulation of apoptosis by the cyclin-dependent kinase inhibitor p27(Kip1).
• The growing role for the cyclin kinase inhibitor p27Kip1 in Renal disease.
• The plasma membrane-actin linking protein, ezrin, is a glomerular epithelial cell marker in glomerulogenesis, in the adult Kidney and in glomerular injury.
• Cell cycle proteins in glomerular Disease.
• Role of intrinsic Renal cells versus infiltrating cells in glomerular crescent formation.
• A new model of Renal microvascular injury.
• The cyclin kinase inhibitor p21WAF1, CIP1 is increased in experimental diabetic Nephropathy: potential role in glomerular hypertrophy.
• The cyclin-dependent kinase inhibitor p27Kip1 safeguards against inflammatory injury.
• CD59 protects glomerular endothelial cells from Immune-mediated thrombotic microangiopathy in rats.
• Accelerated apoptosis characterizes cyclosporine-associated interstitial fibrosis.
• Expression of the cyclin kinase inhibitor, p27kip1, in developing and mature human Kidney.
• Tubulointerstitial disease in aging: evidence for underlying peritubular capillary damage, a potential role for Renal ischemia.

Schools

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• University Of Cape Town

Procedures Preformed

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• Hemodialysis

Conditions Treated

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• Acute Kidney Failure
• Calcium Metabolism Disorders
• Chronic Kidney Diseases
• Diabetes With Renal Manifestations
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Doctors Specialties

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• Nephrology
• Internal Medicine

Accepted Insurances

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• Blue Card PPO
• Cigna HMO
• Cigna PPO
• Great West Healthcare-Cigna PPO
• Open Access Plus
• Commercial Insurance Company
• First Choice Health PPO
• Coop Core
• Connect
• Medicare MCR
• MultiPlan PPO
• ODS Health Plan
• Heritage Plus
• Heritage Signature
• Personal Option EPO
• Preferred Provider Network PPN
• Choice Plus POS
• Navigate HMO
• Navigate POS
• Options PPO

Helpful Reviews

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Medicare Facts

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National Provider Identifier [NPI]	1417032236
Last Name Of The Provider	SHANKLAND
First Name Of The Provider	STUART
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