Past Funding

 

NIH/NIDDK  5 R01 DK083391-01A2 (Alpers)  9/15/2011-8/31/2016      

Podocyte depletion and regeneration during evolution and reversal of diabetic nephropathy

This grant explores mechanisms underlying reversibility (replacement of kidney cell populations that are typically lost in human and experimental diabetic kidney

disease) with emphasis on the podocyte, a unique cell type in the kidney. This grant also focuses on testing new therapies, based on correcting metabolic injuries to

mitochondria (an organelle present within all cells), that are specifically directed to podocyte mitochondria, as a way to promote reversal of diabetic kidney disease

NIH-RO1- Renewal Shankland (PI) 7/1/2011 - 6/30/2016

Cell Cycle and Podocyte Apoptosis

Studies are designed to determine the role of Cyclin I and CDK5, and when active, this complex enhances Survival of terminally differential cells such as podocytes. The

signaling pathways will be delineated. Cell culture and experimental models will be used to delineate this further.

               

NIH/NIDDK   5 R01 DK056799-10 (Shankland)  (9/1/2011-4/30/2016)

 Cell Cycle and Podocytes    

The goal of the first aim of this competitive renewal is to show a new paradigm for cell cycle protein function, based on our preliminary data In summary, the studies

proposed will advance scientific knowledge in glomerular diseases, and in cell cycle protein research. The overall goal of the second aim is to show new regulatory

paradigms for cyclin I-p35-cdk5, which play a fundamental role in glomerular and brain development.   In summary, the studies proposed will advance scientific

knowledge in glomerular diseases, and in cell cycle protein research.
 

NIH-RO1 Shankland (PI) (7/1/10 - 6/30/15)

Podocyte Progenitor Cells

The focus of this grant application is to delineate how terminally differentiated podocyte cell number is Restored following injury in glomerular disease. Based on our

recent data and preliminary data, we have compelling evidence that renin-expressing juxtaglomerular cells and parietal epithelial cells both serve as local progenitor

cells. We will show that they both switch their phenotype in disease, and ultimately become podocytes.
 

American Heart Association 11GRNT7810021 Shankland (PI) (7/1/2011-6/30/13)

Cell Cycle Regulation of Podocyte Proteins

The overall goal of this grant proposal is to prove that both slit diaphragm and actin-binding proteins are Regulated by the cdk5-cyclin I-p35 complex, and that any

alterations in this complex such as occurs in disease, leads to proteinuria and glomerulosclerosis.
 

NIH ARRA Grant (DK056799-07S1) (09/21/09-08/31/11)

Cell Cycle and Podocyte Apoptosis

Studies are designed to determine the role of Cyclin I and CDK5, and when active, this complex enhances survival of terminally differential cells such as podocytes. The

signaling pathways will be delineated. Cell culture and experimental models will be used to delineate this further.
 

NIH R01 Grant (DK056799-05A1) Shankland (PI) (09/30/07 – 6/30/11)

Cell Cycle and Podocyte Apoptosis

The overall goal of this grant is to delineate new paradigms in the regulation of podocyte survival and death, so that ultimately new strategies can be developed to

prevent podocyte loss, enhance kidney survival, and reduce kidney disease.
 

NIH Basic Training Grant (T32 DL07467-21) Shankland(PI) (09/01/2009–8/31/13)

Nephrology Training 03

This is a training grant that supports research training for three M.D. post-graduate fellows who undergo periods of both renal and basic science research training.
 

NIH NIDDK ARRA R21 (DK081835-01A2) Shankland (PI) (08/15/09 – 06/30/11)

New Thoughts on Parietal Cells

The precise biological role of parietal epithelial cells (PECs) are not well understood in health or disease. The main goal of this grant is to show that PECs are required to

limit filtered proteins ‘escaping’ into the peri-glomerular space. We will test the hypotheses that the intra-cellular tight junctions in PECs, together with the underlying

Bowman’s Basement membrane, forms a second barrier to proteinuria. We will also test the hypothesis that PECs actively take up filtered albuminuria which injures

them by inducing apoptosis.
 

1 F32 DK072788-01 Shankland (PI) (9/19/05-12/30/07)

HHS Logar Fellow
 

DHHS 5901 Letter of Credit (LOC) Shankland (PI) (4/1/2008-3/31/09)

7th Intl Podocyte Conference

This grant will be used to support the travel of junior investigators to attend scientific conference.
 

AHA – Established Investigator Award 0340129N Shankland (PI) (1/01/03– 12/31/08)

Role of Cell Cycle in Podocyte Injury

The proposed studies are designed to test novel aspects of cell cycle proteins in disease, so that potential therapeutic interventions can be designed to reduce the

incidence of renal failure.

NIH R01 grant DK 51096-05A2 Shankland (PI) (09/01/04-06/30/07)

Cell Cycle Control in Glomerular Disease

The major goal of this grant is to determine the expression and activity of specific cell cycle proteins in glomerular cell proliferation and differentiation in vitro and in

vivo. Overlap: None.

Applied Molecular Genetics (AMGEN) Shankland (PI) (09/27/04-09/26/06)

Role of Erythropeitin (EPO) in Proteinuria

The overall goal of this grant is to test whether a decrease in endogenous EPO in renal disease augments loss of podocytes differentiation, preventing progressive proteinuria and

scarring.

American Diabetes Association (7-04-RA-107-80-0572) Shankland (PI) (07/01/04-06/30/06)

Role of Podocytes in Diabetic Nephropathy

The overall goal of this grant is to delineate the mechanisms underlying the abnormalities in podocytes, utilizing cultured cells and animal models of diabetic nephropathy.
 

NIH R01 grant DK 60525-02 Shankland (PI) (07/01/02-06/30/06)

Mechanisms of Podocyte Injury

The major goals of this grant are to study the effect of stress-tension-induced injury on podocytes, and also to determine the role of novel cell cycle regulatory proteins in podocyte

disease.
 

NIH R01 grant DK 56799-04 Shankland (PI) (05/01/00-02/28/05)

Cell Cycle Proteins and Glomerular Apoptosis

The major goal of this project is to show novel roles for specific cell cycle proteins in glomerular cell apoptosis beyond that of proliferation.
 

JDRF  1-2001-395 Shankland (PI) (01/01/01-12/31/03)

The Role of Cyclin Kinase Inhibitors in Diabetic Glomerular Hypertrophy

The major goal of this project will be to determine the nuclear mechanisms underlying the development of diabetic hypertrophy, with a focus on specific CDK inhibitors. Overlap: None
.

NIH R01 grant DK 47659-10 Shankland (PI) (09/01/98-08/31/03)

Immunological Renal Diseases: Subproject #2, “The Role of Cell Cycle Proteins in Glomerular Epithelial Cell Growth” 
 

The major goal of this project is to test the hypothesis that specific CDK-inhibitors p57-WT1 determine the proliferative capacity of the glomerular visceral epithelial cell.
 

NIH R01 grant DK 51096 Shankland (PI) (06/01/96-05/31/04)

Cell Cycle Control in Glomerular Disease

The major goal of this grant is to determine the expression and activity of specific cell cycle proteins in glomerular cell proliferation and differentiation in vitro and in vivo.

Overlap: None.
 

NIH/NIDDK R13 (DK069139-01) Shankland (PI) (06/01/04-06/30/05)

“5th International Podocyte Conference”

This grant was used to support the travel of junior investigators to attend this scientific meeting.
 

NIH (R01) Grant; (DK 52121) Shankland (PI) (01/01/97-12/31/01)

Role of the Glomerular Endothelial Cell in Hemolytic Uremic Syndrome (HUS)

The goal was to determine the mechanisms of endothelial cell proliferation and apoptosis.
 

C. V. Therapeutics, Inc. Grant Shankland (PI) (01/01/00-12/31/00)

Role of Cell Cycle Proteins in Hemodialysis Vascular Stenosis

The study was designed to determine the role of cell cycle proteins in vascular access stenosis.