Robert C. Rickert

ORCID: 0000-0003-4292-1708
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About
Contact & Profiles
Research Areas
  • T-cell and B-cell Immunology
  • Immune Cell Function and Interaction
  • Immunotherapy and Immune Responses
  • NF-κB Signaling Pathways
  • Chronic Lymphocytic Leukemia Research
  • PI3K/AKT/mTOR signaling in cancer
  • Monoclonal and Polyclonal Antibodies Research
  • Immune Response and Inflammation
  • Lymphoma Diagnosis and Treatment
  • Cytokine Signaling Pathways and Interactions
  • Ubiquitin and proteasome pathways
  • Protein Tyrosine Phosphatases
  • Galectins and Cancer Biology
  • Immunodeficiency and Autoimmune Disorders
  • FOXO transcription factor regulation
  • Cancer-related Molecular Pathways
  • CAR-T cell therapy research
  • Chronic Myeloid Leukemia Treatments
  • Pancreatic function and diabetes
  • Cell death mechanisms and regulation
  • Diabetes and associated disorders
  • Cell Adhesion Molecules Research
  • Mast cells and histamine
  • Cancer Mechanisms and Therapy
  • Epigenetics and DNA Methylation

Sanford Burnham Prebys Medical Discovery Institute
2012-2022

Discovery Institute
2008-2022

National Cancer Institute
2016-2021

Pfizer (United States)
2018-2021

Max Planck Institute of Immunobiology and Epigenetics
2017

Institute for Medical Research
2006-2009

Abbott (United States)
2009

Rigshospitalet
2008

Northwestern University
2005

University of Turin
2005

A classical cellular response to hypoxia is a cessation of growth. Hypoxia-induced growth arrest differs in different cell types but likely an essential aspect the wounding and injury. An important component hypoxic activation hypoxia-inducible factor 1 (HIF-1) transcription factor. Although this for adaptation low oxygen levels, mechanisms through which it influences cycle arrest, including degree cooperates with tumor suppressor protein p53, remain poorly understood. To determine broadly...

10.1128/mcb.23.1.359-369.2003 article EN Molecular and Cellular Biology 2002-12-13

Non-coding microRNAs (miRs) are a vital component of post-transcriptional modulation protein expression and, like coding mRNAs harbour oncogenic properties. However, the mechanisms governing miR and identity affected transcripts remain poorly understood. Here we identify inositol phosphatase SHIP1 as bonafide target miR-155. We demonstrate that in diffuse large B cell lymphoma (DLBCL) elevated levels miR-155, consequent diminished result autocrine stimulation by pro-inflammatory cytokine...

10.1002/emmm.200900028 article EN cc-by EMBO Molecular Medicine 2009-06-10

Transient transfection of chemically synthesized microRNA (miRNA) mimics is being used extensively to study the functions and mechanisms endogenous miRNAs. However, it remains unclear whether transfected miRNAs behave similarly Here we show that transient miRNA into HeLa cells by a commonly method led accumulation high molecular weight RNA species few hundred fold increase in mature levels. In contrast, expression same through lentiviral infection or plasmid cells, transgenic primary...

10.3389/fgene.2015.00340 article EN cc-by Frontiers in Genetics 2015-12-02

Abstract NF-κB activity in mammalian cells is regulated through the IκB kinase (IKK) complex, consisting of two catalytic subunits (IKKα and IKKβ) a regulatory subunit (IKKγ). Targeted deletion Ikkβ results early embryonic lethality, thus complicating examination IKKβ function adult tissues. Here we describe role B lymphocytes made possible by generation mouse strain that expresses conditional allele. We find loss dramatic reduction all peripheral cell subsets due to associated defects...

10.4049/jimmunol.170.9.4630 article EN The Journal of Immunology 2003-05-01

Genetic ablation of the B cell surface glycoprotein CD19 severely impairs humoral immune response. This requirement is thought to reflect a critical role in signal transduction that occurs upon antigen C3dg coligation receptors with containing type 2 complement (CR2). Here we show plays key accessory receptor signaling independent CR2 and define molecular circuitry by which this function mediated. While not required for antigen-mediated activation proximal tyrosines kinases, it...

10.1084/jem.186.11.1897 article EN The Journal of Experimental Medicine 1997-12-01

BAFF is a soluble factor required for B cell maturation and survival. BAFF-R signals via the noncanonical NF-κB pathway regulated by TRAF3/NIK/IKK1 axis. We show that deletion of Ikk1 during early development causes partial impairment in BAFF-dependent survival, but inactivation mature cells does not affect further employs CD19 to promote survival phosphatidylinositol 3-kinase (PI3K), coinactivation Cd19 profound block at transitional stage. Consistent with role PI3K function, PTEN mediates...

10.1016/j.celrep.2013.10.022 article EN cc-by-nc-nd Cell Reports 2013-11-01
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