ArticleAmerican journal of physiology. Renal physiology2012
Both cyclin I and p35 are required for maximal survival benefit of cyclin-dependent kinase 5 in kidney podocytes.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- The Duality of Cdk5: A Master Regulator in Neurodevelopment and a Hijacked Oncogene in Cancer.Cells · 2025Review
- Article
- Article
- The Effect of Interleukin-4 and Dexamethasone on RNA-Seq-Based Transcriptomic Profiling of Human Podocytes: A Potential Role in Minimal Change Nephrotic Syndrome.Journal of clinical medicine · 2021Article
- Proline-dependent and basophilic kinases phosphorylate human TRPC6 at serine 14 to control channel activity through increased membrane expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- A novel in vivo method to quantify slit diaphragm protein abundance in murine proteinuric kidney disease.PloS one · 2017Article
- Renin-Angiotensin-Aldosterone System Inhibition Increases Podocyte Derivation from Cells of Renin Lineage.Journal of the American Society of Nephrology : JASN · 2016Article
- Partial podocyte replenishment in experimental FSGS derives from nonpodocyte sources.American journal of physiology. Renal physiology · 2016Article
- Knockdown of Expression of Cdk5 or p35 (a Cdk5 Activator) Results in Podocyte Apoptosis.PloS one · 2016Article
- Cells of renin lineage are adult pluripotent progenitors in experimental glomerular disease.American journal of physiology. Renal physiology · 2015Article
- Changes in glomerular parietal epithelial cells in mouse kidneys with advanced age.American journal of physiology. Renal physiology · 2015Article
- ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2015Article
- Cells of renin lineage take on a podocyte phenotype in aging nephropathy.American journal of physiology. Renal physiology · 2014Article
- Role of CDK5/cyclin complexes in ischemia-induced death and survival of renal tubular cells.Cell cycle (Georgetown, Tex.) · 2014Article
- Cells of renin lineage are progenitors of podocytes and parietal epithelial cells in experimental glomerular disease.The American journal of pathology · 2013Article
- Cdk5: An Emerging Kinase in Pain Signaling.Brain disorders & therapy · 2013Article
- Podocyte repopulation by renal progenitor cells following glucocorticoids treatment in experimental FSGS.American journal of physiology. Renal physiology · 2013Article
- Reversibility of structural and functional damage in a model of advanced diabetic nephropathy.Journal of the American Society of Nephrology : JASN · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Cyclin-dependent kinase (Cdk)-5 is activated by both cyclin I and the noncyclin activator p35 in terminally differentiated cells such as kidney podocytes and neurons. Cyclin I and p35 are restricted to podocytes in the kidney, and each limit podocyte apoptosis by activating Cdk5. To determine whether both activators are necessary, or whether they serve backup roles, a double cyclin I-p35 null mouse was generated. Experimental glomerular disease characterized by podocyte apoptosis was then induced by administering an anti-podocyte antibody. The results showed that under nonstressed conditions double mutants had normal kidney structure and function and were indistinguishable from wild-type, cyclin I(-/-), or p35(-/-) mice. In contrast, when stressed with disease, podocyte apoptosis increased fourfold compared with diseased cyclin I(-/-) or p35(-/-) mice. This resulted in a more pronounced decrease in podocyte number, proteinuria, and glomerulosclerosis. Under normal states and nephritic states, levels for the prosurvival protein Bcl-2 were lower in double cyclin I(-/-) p35(-/-) mice than the other mice. Similarly, levels of Bcl-xL, another prosurvival member, were lower in normal and nephritic double cyclin I(-/-) p35(-/-) mice but similar to single-cyclin I(-/-) mice. Moreover, levels of ERK1/2 and MEK1/2 activation were lower in nephritic double cyclin I(-/-) p35(-/-) mice but similar to single-cyclin I(-/-) mice. The results demonstrate that the activators of Cdk5, p35, and cyclin I are not required for normal kidney function. However, they play pivotal coordinated roles in maintaining podocyte survival during stress states in disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.