KrasG12D-induced IKK2/β/NF-κB activation by IL-1α and p62 feedforward loops is required for development of pancreatic ductal adenocarcinoma. (Q35990138)

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English	KrasG12D-induced IKK2/β/NF-κB activation by IL-1α and p62 feedforward loops is required for development of pancreatic ductal adenocarcinoma.	scientific article

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20 January 2020

KrasG12D-induced IKK2/β/NF-κB activation by IL-1α and p62 feedforward loops is required for development of pancreatic ductal adenocarcinoma (English)

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Huamin Wang

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Jason B Fleming

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Mien-Chie Hung

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Bailu Peng

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Jianhua Ling

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Ya'an Kang

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Ruiying Zhao

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Qianghua Xia

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Zhe Chang

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Jin Li

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Jinsong Liu

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Ihor R Lemischka

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Paul J Chiao

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1 January 2012

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1

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105-120

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20 January 2020

Defective feedback regulation of NF-kappaB underlies Sjogren's syndrome in mice with mutated kappaB enhancers of the IkappaBalpha promoter

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Conditional ablation of Ikkb inhibits melanoma tumor development in mice

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Requirement of the NF-kappaB subunit p65/RelA for K-Ras-induced lung tumorigenesis

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Hepatocyte IKKbeta/NF-kappaB inhibits tumor promotion and progression by preventing oxidative stress-driven STAT3 activation

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Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1

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Requirement for NF-kappaB signalling in a mouse model of lung adenocarcinoma

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The signaling adaptor p62 is an important NF-kappaB mediator in tumorigenesis

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The IkappaB kinase - a bridge between inflammation and cancer

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NF-kappaB is a negative regulator of IL-1beta secretion as revealed by genetic and pharmacological inhibition of IKKbeta

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IKK beta suppression of TSC1 links inflammation and tumor angiogenesis via the mTOR pathway

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RalB GTPase-mediated activation of the IkappaB family kinase TBK1 couples innate immune signaling to tumor cell survival

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Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse

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The p62 scaffold regulates nerve growth factor-induced NF-kappaB activation by influencing TRAF6 polyubiquitination

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In vitro modeling of human pancreatic duct epithelial cell transformation defines gene expression changes induced by K-ras oncogenic activation in pancreatic carcinogenesis

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Notch 2-positive progenitors with the intrinsic ability to give rise to pancreatic ductal cells

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Inhibition of mammalian target of rapamycin reverses alveolar epithelial neoplasia induced by oncogenic K-ras

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IkappaB kinase promotes tumorigenesis through inhibition of forkhead FOXO3a

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Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma

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Inhibition of constitutive NF-kappa B activity by I kappa B alpha M suppresses tumorigenesis

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Direct evidence for the pancreatic lineage: NGN3+ cells are islet progenitors and are distinct from duct progenitors

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IKKβ Is Required for Peripheral B Cell Survival and Proliferation

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12 December 2020

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The nuclear factor-kappa B RelA transcription factor is constitutively activated in human pancreatic adenocarcinoma cells

1 reference

https://pubmed.ncbi.nlm.nih.gov/22264792

12 December 2020

based on heuristic

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Early diagnosis and treatment of pancreatic dysplasia in patients with a family history of pancreatic cancer

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https://pubmed.ncbi.nlm.nih.gov/22264792

12 December 2020

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10.1016/J.CCR.2011.12.006

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release_k4z4xsabmrdojoesvazbtilk5q

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24 November 2022

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20 January 2020

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20 January 2020

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