What is he best known for?
The fields of study he is best known for:
- Gene
- Internal medicine
- Biochemistry
Endocrinology, Internal medicine, Cell biology, Biochemistry and Endocytosis are his primary areas of study.
As part of his studies on Endocrinology, Michael Gekle often connects relevant subjects like Receptor.
His Internal medicine research includes elements of Extracellular, Intracellular pH, Organic anion transporter 1 and Downregulation and upregulation.
Michael Gekle is interested in Kinase, which is a field of Cell biology.
His study in Biochemistry is interdisciplinary in nature, drawing from both Cell culture, Kidney metabolism, In vivo and Pharmacology.
His Endocytosis research includes themes of Reabsorption, Protein kinase C and Endosome.
His most cited work include:
- Renal tubule albumin transport. (210 citations)
- Characterization of two MDCK-cell subtypes as a model system to study principal cell and intercalated cell properties. (179 citations)
- Cubilin- and megalin-mediated uptake of albumin in cultured proximal tubule cells of opossum kidney (164 citations)
What are the main themes of his work throughout his whole career to date?
The scientist’s investigation covers issues in Internal medicine, Endocrinology, Cell biology, Biochemistry and Kidney.
He regularly ties together related areas like Signal transduction in his Internal medicine studies.
As a part of the same scientific study, Michael Gekle usually deals with the Endocrinology, concentrating on Receptor and frequently concerns with Transactivation.
His Cell biology research focuses on Endocytosis and how it relates to Albumin and Endosome.
His Biochemistry study combines topics in areas such as Molecular biology and Cell culture.
The various areas that Michael Gekle examines in his Kidney study include Organic anion transporter 1, Ochratoxin A and Ion transporter.
He most often published in these fields:
- Internal medicine (39.05%)
- Endocrinology (38.10%)
- Cell biology (30.48%)
What were the highlights of his more recent work (between 2014-2021)?
- Endocrinology (38.10%)
- Internal medicine (39.05%)
- Cell biology (30.48%)
In recent papers he was focusing on the following fields of study:
Michael Gekle mostly deals with Endocrinology, Internal medicine, Cell biology, Vascular smooth muscle and Mineralocorticoid receptor.
His study in Lipopolysaccharide and Nifedipine are all subfields of Internal medicine.
His biological study spans a wide range of topics, including Cell culture, Transcriptome, microRNA, Proinflammatory cytokine and Programmed cell death.
His work deals with themes such as Extracellular, Extracellular matrix and Kidney, which intersect with Cell culture.
His Mineralocorticoid receptor research is multidisciplinary, incorporating perspectives in Cirrhosis and Hypoxia.
Michael Gekle combines subjects such as Aldosterone, Renal damage, Tissue homeostasis and Heart rate with his study of Epidermal growth factor receptor.
Between 2014 and 2021, his most popular works were:
- Acidic environment activates inflammatory programs in fibroblasts via a cAMP–MAPK pathway (42 citations)
- Kidney and aging - A narrative review. (29 citations)
- Acidosis Promotes Metastasis Formation by Enhancing Tumor Cell Motility. (25 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Internal medicine
- Biochemistry
His scientific interests lie mostly in Cell culture, Molecular biology, Cell biology, Internal medicine and Endocrinology.
His study in Cell culture is interdisciplinary in nature, drawing from both Cancer research, Tumor microenvironment, RNA, Cell adhesion and Motility.
His work deals with themes such as HEK 293 cells and Proteome, which intersect with Molecular biology.
His Cell biology study combines topics in areas such as Transcriptome, Downregulation and upregulation, Post-transcriptional regulation, Caspase and microRNA.
Internal medicine is often connected to Tissue homeostasis in his work.
His Renal function research integrates issues from Acute kidney injury, Nitric oxide, Ischemia and Renal ischemia.
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