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Crosstalk between KDEL receptor and EGF receptor mediates cell proliferation and migration via STAT3 signaling Open
Hostile microenvironment of cancer cells provoke a stressful condition for endoplasmic reticulum (ER) and stimulate the expression and secretion of ER chaperones, leading to tumorigenic effects. However, the molecular mechanism underlying …
Crosstalk between KDEL receptor and EGF receptor mediates cell proliferation and migration via STAT3 signaling Short title: KDELR regulates EGFR-STAT3 signaling Open
Hostile microenvironment of cancer cells provoke a stressful condition for endoplasmic reticulum (ER) and stimulate the expression and secretion of ER chaperones, leading to tumorigenic effects. However, the molecular mechanism underlying …
An A-kinase anchoring protein (ACBD3) coordinates traffic-induced PKA activation at the Golgi Open
KDEL receptor (KDELR) is a key protein that recycles escaped endoplasmic reticulum (ER) resident proteins from the Golgi apparatus back to the ER and maintains a dynamic balance between these two organelles in the early secretory pathway. …
KDEL Receptor Trafficking to the Plasma Membrane Is Regulated by ACBD3 and Rab4A-GTP Open
KDEL receptor-1 maintains homeostasis in the early secretory pathway by capturing and retrieving ER chaperones to the ER during heavy secretory activity. Unexpectedly, a fraction of the receptor is also known to reside in the plasma membra…
Crosstalk between KDEL receptor and EGF receptor mediates cell proliferation and migration via STAT3 signaling Open
Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that hosts complex signaling events and plays diverse roles in a variety of cellular processes. Secreted ER chaperones are capable of activating EGFR and its downstream …
KDEL Receptor Trafficking to the Plasma Membrane is Regulated by ACBD3 and Rab4-GTP Open
KDEL receptor-1 maintains homeostasis in the early secretory pathway by capturing and retrieving ER-chaperones to the ER during heavy secretory activity. We have previously shown that a Golgi scaffolding protein (ACBD3) facilitates KDEL re…
Retro-2 Alters Golgi Structure and Function Open
Retro-2 directly interacts with an ER exit site protein, Sec16A, inhibiting ER exit of a Golgi tSNARE, Syntaxin5, which results in rapid re-distribution of Syntaxin5 to the ER. Recently, it was shown that SARS-CoV-2 infection disrupts the …
ACBD3 modulates KDEL receptor interaction with PKA for its trafficking via tubulovesicular carrier Open
Background KDEL receptor helps establish cellular equilibrium in the early secretory pathway by recycling leaked ER-chaperones to the ER during secretion of newly synthesized proteins. Studies have also shown that KDEL receptor may functio…
Additional file 10 of ACBD3 modulates KDEL receptor interaction with PKA for its trafficking via tubulovesicular carrier Open
Additional file 10. KDELR-BioID Mass Spectrometry Data.