Modulating EGFR-MTORC1-autophagy as a potential therapy for persistent fetal vasculature (PFV) disease.
Meysam YazdankhahPeng ShangSayan GhoshImran A BhuttoNadezda StepichevaRhonda GrebeStacey HoseJoseph WeissTianqi LuoSubrata MishraS Amer RiazuddinArkasubhra GhoshJames T HandaGerard A LuttyJ Samuel ZiglerDebasish SinhaPublished in: Autophagy (2019)
ACTB: actin, beta; CCND3: cyclin 3; CDK6: cyclin-dependent kinase 6; CHQ: chloroquine; COL4A1: collagen, type IV, alpha 1; CRYBA1: crystallin, beta A1; DAPI: 4'6-diamino-2-phenylindole; EGFR: epidermal growth factor receptor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFAP: glial fibrillary growth factor; KDR: kinase insert domain protein receptor; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MKI67: antigen identified by monoclonal antibody Ki 67; MTORC1: mechanistic target of rapamycin kinase complex 1; PARP: poly (ADP-ribose) polymerase family; PCNA: proliferating cell nuclear antigen; PFV: persistent fetal vasculature; PHPV: persistent hyperplastic primary vitreous; RPE: retinal pigmented epithelium; RPS6: ribosomal protein S6; RPS6KB1: ribosomal protein S6 kinase, polypeptide 1; SQSTM1/p62: sequestome 1; TUBB: tubulin, beta; VCL: vinculin; VEGFA: vascular endothelial growth factor A; WT: wild type.
Keyphrases
- epidermal growth factor receptor
- tyrosine kinase
- growth factor
- vascular endothelial growth factor
- monoclonal antibody
- advanced non small cell lung cancer
- protein kinase
- small cell lung cancer
- cell cycle
- wild type
- protein protein
- amino acid
- cell death
- mass spectrometry
- signaling pathway
- stem cells
- oxidative stress
- diabetic retinopathy
- spinal cord injury
- endothelial cells
- squamous cell carcinoma
- radiation therapy
- high resolution
- cell migration
- neuropathic pain
- neoadjuvant chemotherapy
- cell proliferation
- climate change
- bone marrow
- structural basis
- spinal cord
- high resolution mass spectrometry
- locally advanced