Vladimir Kirkin

ORCID: 0000-0002-8049-3663
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About
Contact & Profiles
Research Areas
  • CAR-T cell therapy research
  • Immune Cell Function and Interaction
  • Immunotherapy and Immune Responses
  • Autophagy in Disease and Therapy
  • MicroRNA in disease regulation
  • Cancer-related molecular mechanisms research
  • Circular RNAs in diseases
  • Ubiquitin and proteasome pathways
  • Endoplasmic Reticulum Stress and Disease
  • RNA Interference and Gene Delivery
  • Cell death mechanisms and regulation
  • Cancer Immunotherapy and Biomarkers
  • Cannabis and Cannabinoid Research
  • Phagocytosis and Immune Regulation
  • Angiogenesis and VEGF in Cancer
  • Lymphatic System and Diseases
  • Protein Degradation and Inhibitors
  • Calcium signaling and nucleotide metabolism
  • Peptidase Inhibition and Analysis
  • Cancer-related Molecular Pathways
  • Colorectal Cancer Treatments and Studies
  • Mitochondrial Function and Pathology
  • DNA and Nucleic Acid Chemistry
  • DNA Repair Mechanisms
  • Ultrasound and Hyperthermia Applications

Molecular Partners (Switzerland)
2021-2024

Institute of Cancer Research
2016-2024

Cancer Research UK
2016-2022

Merck (Germany)
2010-2017

Georg Speyer Haus
2003-2010

Goethe University Frankfurt
2007-2010

FZI Research Center for Information Technology
2001-2005

University Hospital Schleswig-Holstein
2005

University of Lübeck
2005

Centre d’Immunologie de Marseille-Luminy
2005

Autophagy is an evolutionary conserved cell survival process for degradation of long-lived proteins, damaged organelles and protein aggregates. The mammalian proteins p62 NBR1 are selectively degraded by autophagy can act as cargo receptors or adaptors the autophagic ubiquitinated substrates. Despite differing in size primary sequence, both share a similar domain architecture containing N-terminal PB1 domain, LIR motif interacting with ATG8 family C-terminal UBA ubiquitin. essential their...

10.4161/cc.8.13.8892 article EN Cell Cycle 2009-07-01

Autophagy is a lysosome-dependent degradation system conserved among eukaryotes. The mammalian Atg1 homologues, Unc-51 like kinase (ULK) 1 and 2, are multifunctional proteins with roles in autophagy, neurite outgrowth, vesicle transport. ULK complex involved autophagy consists of ULK1, ULK2, ATG13, FIP200, ATG101. We have used pulldown peptide array overlay assays to study interactions between the six different ATG8 family proteins. Strikingly, addition ULK1 ATG13 FIP200 interacted human...

10.1074/jbc.m112.378109 article EN cc-by Journal of Biological Chemistry 2012-10-06

Macroautophagy/autophagy is an evolutionarily conserved pathway responsible for clearing cytosolic aggregated proteins, damaged organelles or invading microorganisms. Dysfunctional autophagy leads to pathological accumulation of the cargo, which has been linked a range human diseases, including neurodegenerative infectious and autoimmune diseases various forms cancer. Cumulative work in animal models, application genetic tools pharmacologically active compounds, suggested potential...

10.1080/15548627.2021.1936359 article EN cc-by-nc-nd Autophagy 2021-07-09

Selective degradation of intracellular targets, such as misfolded proteins and damaged organelles, is an important homeostatic function that autophagy has acquired in addition to its more general role restoring the nutrient balance during stress starvation. Although exact mechanism underlying selection autophagic substrates not known, ubiquitination a candidate signal for aggregated proteins. p62/SQSTM1 was first protein shown bind both target-associated ubiquitin (Ub) LC3 conjugated...

10.4161/auto.5.5.8566 article EN Autophagy 2009-07-01

Physical and chemical DNA-damaging agents are used widely in the treatment of cancer. Double-strand break (DSB) lesions DNA most deleterious form damage and, if left unrepaired, can effectively kill cancer cells. DNA-dependent protein kinase (DNA-PK) is a critical component nonhomologous end joining (NHEJ), one two major pathways for DSB repair. Although DNA-PK has been considered an attractive target therapy, development pharmacologic inhibitors clinical use lagging. Here, we report...

10.1158/1535-7163.mct-19-0734 article EN Molecular Cancer Therapeutics 2020-03-27

Macroautophagy/autophagy can enable cancer cells to withstand cellular stress and maintain bioenergetic homeostasis by sequestering components into newly formed double-membrane vesicles destined for lysosomal degradation, potentially affecting the efficacy of anti-cancer treatments. Using 13C-labeled choline 13C-magnetic resonance spectroscopy western blotting, we show increased de novo phospholipid (ChoPL) production activation PCYT1A (phosphate cytidylyltransferase 1, choline, alpha),...

10.1080/15548627.2019.1659608 article EN cc-by Autophagy 2019-09-13

Abstract Purpose: The multi-kinase inhibitor (mKi) regorafenib has demonstrated efficacy in chemorefractory patients with metastatic colorectal cancer (mCRC). However, lack of predictive biomarkers and concerns over significant toxicities hamper the use clinical practice. Experimental Design: Serial liquid biopsies were obtained at baseline monthly until disease progression mCRC treated a phase II trial (PROSPECT-R n = 40; NCT03010722) multicentric validation cohort (n 241). Tissue collected...

10.1158/1078-0432.ccr-23-2748 article EN Clinical Cancer Research 2024-02-20
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