Cell Signaling Technology

ULK1 Antibody Sampler Kit

#8359 · $650

65
Evidence Score · Well-Established
Used by 480 independent labs across 505 papers. How we score this →
100
Citing papers
5.4k
Combined citations
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Research areas

Cell death mechanisms and regulation18interferon and immune responses9Autophagy in Disease and Therapy9Cancer-related molecular mechanisms research8RNA modifications and cancer6Immune Response and Inflammation6Influenza Virus Research Studies6RNA Research and Splicing6

Papers citing this product

1
Single-nucleus analysis of accessible chromatin in developing mouse forebrain reveals cell-type-specific transcriptional regulation
Nature Neuroscience·2018·388 cit.·DOI
2
Overlapping cleavage motif selectivity of caspases: implications for analysis of apoptotic pathways
Cell Death and Differentiation·2007·310 cit.·DOI
3
Influenza A virus protein PB1-F2 translocates into mitochondria via Tom40 channels and impairs innate immunity
Nature Communications·2014·250 cit.·DOI
4
Ordering of caspases in cells undergoing apoptosis by the intrinsic pathway
Cell Death and Differentiation·2009·245 cit.·DOI
5
Inducible Dimerization and Inducible Cleavage Reveal a Requirement for Both Processes in Caspase-8 Activation
Journal of Biological Chemistry·2010·211 cit.·DOI
6
A Caspase Cascade Regulating Developmental Axon Degeneration
Journal of Neuroscience·2012·207 cit.·DOI
7
Caspase-12 and Caspase-4 Are Not Required for Caspase-dependent Endoplasmic Reticulum Stress-induced Apoptosis
Journal of Biological Chemistry·2005·175 cit.·DOI
8
The PB1 protein of influenza A virus inhibits the innate immune response by targeting MAVS for NBR1-mediated selective autophagic degradation
PLoS Pathogens·2021·144 cit.·DOI
9
XIAP inhibition of caspase-3 preserves its association with the Apaf-1 apoptosome and prevents CD95- and Bax-induced apoptosis
Cell Death and Differentiation·2002·125 cit.·DOI
10
HuR biological function involves RRM3-mediated dimerization and RNA binding by all three RRMs
Nucleic Acids Research·2018·122 cit.·DOI

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