Synthetic amyloid beta does not induce a robust transcriptional response in innate immune cell culture systems

to related objects

Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1742-2094

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Synthetic amyloid beta does not induce a robust transcriptional response in innate immune cell culture systems ; volume:19 ; number:1 ; day:23 ; month:4 ; year:2022 ; pages:1-12 ; date:12.2022
Journal of neuroinflammation ; 19, Heft 1 (23.4.2022), 1-12, 12.2022

Creator: Quiroga, I. Y.
Cruikshank, A. E.
Bond, M. L.
Reed, K. S. M.
Evangelista, B. A.
Tseng, J. H.
Ragusa, J. V.
Meeker, R. B.
Won, H.
Cohen, S.
Cohen, T. J.
Phanstiel, D. H.

Contributor: SpringerLink (Online service)

DOI: 10.1186/s12974-022-02459-1

URN: urn:nbn:de:101:1-2022070618555231090350

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:20 AM CEST

Data provider

This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.

Show original at data provider

Associated

Quiroga, I. Y.
Cruikshank, A. E.
Bond, M. L.
Reed, K. S. M.
Evangelista, B. A.
Tseng, J. H.
Ragusa, J. V.
Meeker, R. B.
Won, H.
Cohen, S.
Cohen, T. J.
Phanstiel, D. H.
SpringerLink (Online service)

Other Objects (12)

Transcriptional regulators dictate innate lymphoid cell fates

Hochschulschrift

Transcriptional networks regulating innate lymphoid cell fate decisions

Mechanistic insights into the role of amyloid-β in innate immunity

Ribonuclease H2 mutations induce a cGAS/STING ‐dependent innate immune response

TLR9 and STING agonists synergistically induce innate and adaptive type‐II IFN

Amyloidogenic amyloid-β-peptide variants induce microbial agglutination and exert antimicrobial activity

Synthetic Rhamnolipid Bolaforms trigger an innate immune response in Arabidopsis thaliana

β-Turn mimetic synthetic peptides as amyloid-β aggregation inhibitors

Transcriptional profiling uncovers human hyalocytes as a unique innate immune cell population

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

HIV-1 counteracts an innate restriction by amyloid precursor protein resulting in neurodegeneration

Transcriptional regulators dictate innate lymphoid cell fates

Hochschulschrift

Transcriptional networks regulating innate lymphoid cell fate decisions

Mechanistic insights into the role of amyloid-β in innate immunity

Ribonuclease H2 mutations induce a cGAS/STING ‐dependent innate immune response

TLR9 and STING agonists synergistically induce innate and adaptive type‐II IFN

Amyloidogenic amyloid-β-peptide variants induce microbial agglutination and exert antimicrobial activity

Synthetic Rhamnolipid Bolaforms trigger an innate immune response in Arabidopsis thaliana

β-Turn mimetic synthetic peptides as amyloid-β aggregation inhibitors

Transcriptional profiling uncovers human hyalocytes as a unique innate immune cell population

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

HIV-1 counteracts an innate restriction by amyloid precursor protein resulting in neurodegeneration

Transcriptional regulators dictate innate lymphoid cell fates

Hochschulschrift

Transcriptional networks regulating innate lymphoid cell fate decisions

Mechanistic insights into the role of amyloid-β in innate immunity

Ribonuclease H2 mutations induce a cGAS/STING ‐dependent innate immune response

TLR9 and STING agonists synergistically induce innate and adaptive type‐II IFN

Amyloidogenic amyloid-β-peptide variants induce microbial agglutination and exert antimicrobial activity

Synthetic Rhamnolipid Bolaforms trigger an innate immune response in Arabidopsis thaliana

β-Turn mimetic synthetic peptides as amyloid-β aggregation inhibitors

Transcriptional profiling uncovers human hyalocytes as a unique innate immune cell population

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

HIV-1 counteracts an innate restriction by amyloid precursor protein resulting in neurodegeneration

Cultural heritage institutions wishing to register will find more information here.

Fields marked * need to be filled in.

Username*

Please enter your username

Email*

Please enter your email address

Please do not fill this field

First name

Last name

Password*

Please enter your password

Confirm password*

Please enter the same password

I have read the terms of use and the privacy policy for the collection of personal data and accept them. *

This field is required.

I would like to subscribe to the newsletter of the Deutsche Digitale Bibliothek. See newsletter subscription info.

Account created

Your "My DDB" account has been successfully created. Before you can log in to your account, you must click the confirmation link in the message we just sent to the email address you provided.

Synthetic amyloid beta does not induce a robust transcriptional response in innate immune cell culture systems

Object Details

References and Relationships

Contributors, Places and Time

Further information

Data provider

Associated

Other Objects (12)

Transcriptional regulators dictate innate lymphoid cell fates

Transcriptional networks regulating innate lymphoid cell fate decisions

Mechanistic insights into the role of amyloid-β in innate immunity

Ribonuclease H2 mutations induce a cGAS/STING ‐dependent innate immune response

TLR9 and STING agonists synergistically induce innate and adaptive type‐II IFN

Amyloidogenic amyloid-β-peptide variants induce microbial agglutination and exert antimicrobial activity

Synthetic Rhamnolipid Bolaforms trigger an innate immune response in Arabidopsis thaliana

β-Turn mimetic synthetic peptides as amyloid-β aggregation inhibitors

Transcriptional profiling uncovers human hyalocytes as a unique innate immune cell population

Transcriptional profiling uncovers human hyalocytes as a unique innate immune cell population

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

HIV-1 counteracts an innate restriction by amyloid precursor protein resulting in neurodegeneration

Transcriptional regulators dictate innate lymphoid cell fates

Transcriptional networks regulating innate lymphoid cell fate decisions

Mechanistic insights into the role of amyloid-β in innate immunity

Ribonuclease H2 mutations induce a cGAS/STING ‐dependent innate immune response

TLR9 and STING agonists synergistically induce innate and adaptive type‐II IFN

Amyloidogenic amyloid-β-peptide variants induce microbial agglutination and exert antimicrobial activity

Synthetic Rhamnolipid Bolaforms trigger an innate immune response in Arabidopsis thaliana

β-Turn mimetic synthetic peptides as amyloid-β aggregation inhibitors

Transcriptional profiling uncovers human hyalocytes as a unique innate immune cell population

Transcriptional profiling uncovers human hyalocytes as a unique innate immune cell population

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

HIV-1 counteracts an innate restriction by amyloid precursor protein resulting in neurodegeneration

Transcriptional regulators dictate innate lymphoid cell fates

Transcriptional networks regulating innate lymphoid cell fate decisions

Mechanistic insights into the role of amyloid-β in innate immunity

Ribonuclease H2 mutations induce a cGAS/STING ‐dependent innate immune response

TLR9 and STING agonists synergistically induce innate and adaptive type‐II IFN

Amyloidogenic amyloid-β-peptide variants induce microbial agglutination and exert antimicrobial activity

Synthetic Rhamnolipid Bolaforms trigger an innate immune response in Arabidopsis thaliana

β-Turn mimetic synthetic peptides as amyloid-β aggregation inhibitors

Transcriptional profiling uncovers human hyalocytes as a unique innate immune cell population

Transcriptional profiling uncovers human hyalocytes as a unique innate immune cell population

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

HIV-1 counteracts an innate restriction by amyloid precursor protein resulting in neurodegeneration

Related objects

Reset password