Heather Maecker

ORCID: 0000-0002-5378-1141
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About
Contact & Profiles
Research Areas
  • Synthesis and Characterization of Heterocyclic Compounds
  • Cancer-related Molecular Pathways
  • Cell death mechanisms and regulation
  • Bioactive Compounds and Antitumor Agents
  • Cancer Immunotherapy and Biomarkers
  • Metal complexes synthesis and properties
  • Immune Cell Function and Interaction
  • Ubiquitin and proteasome pathways
  • Multiple Myeloma Research and Treatments
  • Cancer Mechanisms and Therapy
  • NF-κB Signaling Pathways
  • CAR-T cell therapy research
  • Microtubule and mitosis dynamics
  • interferon and immune responses
  • Birth, Development, and Health
  • Autophagy in Disease and Therapy
  • Cancer therapeutics and mechanisms
  • Phagocytosis and Immune Regulation
  • Peptidase Inhibition and Analysis
  • Melanoma and MAPK Pathways
  • Immune cells in cancer
  • Prenatal Substance Exposure Effects
  • Reproductive System and Pregnancy
  • HER2/EGFR in Cancer Research
  • Peroxisome Proliferator-Activated Receptors

Stanford University
1996-2017

University College London
2016

Genentech
2013-2014

University of Chicago
2011

May Institute
2011

Abbott (United States)
2011

Translational Research in Oncology
2009

Molecular Oncology (United States)
2005

Stanford Medicine
2000-2002

Loyola University Chicago
1993

Apo2 ligand/tumor necrosis factor (TNF)-related apoptosis-inducing ligand (Apo2L/TRAIL) mainly activates programmed cell death through caspases. By contrast, TNF primarily induces gene transcription the inhibitor of κB kinase (IKK), c-Jun N-terminal (JNK), and p38 mitogen-activated protein pathways. Apo2L/TRAIL also can stimulate these kinases, albeit less strongly; however, underlying mechanisms this stimulation its relation to apoptosis are not well understood. Here we show that pathways...

10.1074/jbc.m509560200 article EN cc-by Journal of Biological Chemistry 2005-10-17

Signaling downstream of tumor necrosis factor family receptors hinges on the presence or absence c-IAP proteins.

10.1126/scisignal.2001878 article EN Science Signaling 2012-03-20

The ability of a cancer cell to avoid apoptosis is crucial tumorigenesis and can also contribute chemoresistance. Bcl-2 family prosurvival proteins (Bcl-2, Bcl-X(L), Bcl-w, Mcl-1, A1) plays key role in these processes. We previously reported the discovery ABT-263 (navitoclax), potent small-molecule inhibitor Bcl-2, Bcl-w. While navitoclax exhibits single-agent activity tumors dependent on or Bcl-X(L) for survival, expression Mcl-1 has been shown confer resistance navitoclax, most notably...

10.1158/1535-7163.mct-11-0415 article EN Molecular Cancer Therapeutics 2011-09-14

Corticotropin-releasing factor (CRF), the principle hypothalamic regulator of adrenocortical axis, also functions as a neurotransmitter. In this latter role, CRF causes electrophysiological activation and epileptiform activity in various brain regions. That finding, coupled with observation that mRNA is induced endangered regions following necrotic insults, suggests peptide might contribute to neuron loss. Supporting that, number studies have shown antagonists decrease ischemic or...

10.1016/s0006-8993(96)01207-3 article EN cc-by-nc-nd Brain Research 1997-01-01

10.1016/0165-3806(93)90221-u article EN Developmental Brain Research 1993-12-01

Meeting abstracts Pharmacological inhibition of the MAPK pathway with MEK or BRAF antagonists has proved successful in inducing regression melanoma tumors bearing targeted activating mutations. Moreover, antibodies targeting T-cell immune checkpoint inhibitors CTLA-4 PD-L1/PD-1 have

10.1186/2051-1426-1-s1-p79 article EN cc-by Journal for ImmunoTherapy of Cancer 2013-11-01
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