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Martin Lotz

Researcher at Scripps Research Institute

Publications -  382
Citations -  33862

Martin Lotz is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Cartilage & Chondrocyte. The author has an hindex of 97, co-authored 343 publications receiving 30942 citations. Previous affiliations of Martin Lotz include Japan Agency for Medical Research and Development & University of California, San Diego.

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Journal Article

Proliferating cell nuclear antigen (PCNA)/cyclin in activated human T lymphocytes.

TL;DR: The results show that PCNA expression is regulated by a signal after IL 2 binding and thatPCNA labeling is a precise indicator for human T cells that are committed to DNA synthesis.
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Mohawk promotes the maintenance and regeneration of the outer annulus fibrosus of intervertebral discs

TL;DR: It is shown that homeobox protein Mohawk (Mkx) is a key transcription factor that regulates AF development, maintenance and regeneration and that Mesenchymal stem cells overexpressing Mkx promote functional AF regeneration in a mouse AF defect model.
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Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy

TL;DR: FN, a PPARα agonist used for dyslipidaemias in humans, reduced the number of senescent cells via apoptosis, increased autophagic flux, and protected against cartilage degradation in both ageing human and OA chondrocytes.
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Expression of prepro-enkephalin in human articular chondrocytes is linked to cell proliferation.

TL;DR: In this article, it was shown that cultured human articular chondrocytes express high levels of 1.4 kb prepro-enkephalin mRNA, but not in confluent, contact-inhibited cells.
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Focal adhesion kinase and mitogen-activated protein kinases are involved in chondrocyte activation by the 29-kDa amino-terminal fibronectin fragment.

TL;DR: It is demonstrated that FN-f induced nitric oxide (NO) production from human articular chondrocytes and the effect of IL-1 receptor antagonist (IL-1ra) and mitogen-activated protein kinases showed activation of extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase, and p38 MAPK.