Cell Signaling Technology

SMAD5 Antibody

#9517 · $136,317

65

Evidence Score · Well-Established

Used by 196 independent labs across 204 papers. How we score this →

100

Citing papers

6.1k

Combined citations

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Research areas

Immune cells in cancer15 Endoplasmic Reticulum Stress and Disease9 Immune Cell Function and Interaction7 Epigenetics and DNA Methylation6 Parathyroid Disorders and Treatments5 Autophagy in Disease and Therapy5 Developmental Biology and Gene Regulation4 Genomics, phytochemicals, and oxidative stress4

Papers citing this product

1

Implications of the tumor immune microenvironment for staging and therapeutics

Modern Pathology·2017·364 cit.·DOI

2

Microbial metabolite butyrate facilitates M2 macrophage polarization and function

Scientific Reports·2016·313 cit.·DOI

3

Nucleoporin NUP153 Phenylalanine-Glycine Motifs Engage a Common Binding Pocket within the HIV-1 Capsid Protein to Mediate Lentiviral Infectivity

PLoS Pathogens·2013·294 cit.·DOI

4

Blocking immunoinhibitory receptor LILRB2 reprograms tumor-associated myeloid cells and promotes antitumor immunity

Journal of Clinical Investigation·2018·262 cit.·DOI

5

MicroRNA-155 Promotes Autophagy to Eliminate Intracellular Mycobacteria by Targeting Rheb

PLoS Pathogens·2013·254 cit.·DOI

6

Macrophages are recruited to hypoxic tumor areas and acquire a Pro-Angiogenic M2-Polarized phenotype via hypoxic cancer cell derived cytokines Oncostatin M and Eotaxin

Oncotarget·2014·223 cit.·DOI

7

A promising biodegradable magnesium alloy suitable for clinical vascular stent application

Scientific Reports·2017·167 cit.·DOI

8

Chemerin aggravates DSS-induced colitis by suppressing M2 macrophage polarization

Cellular and Molecular Immunology·2014·165 cit.·DOI

9

Fbxw7 increases CCL2/7 in CX3CR1hi macrophages to promote intestinal inflammation

Journal of Clinical Investigation·2019·145 cit.·DOI

10

Myeloid-Specific Rictor Deletion Induces M1 Macrophage Polarization and Potentiates In Vivo Pro-Inflammatory Response to Lipopolysaccharide

PLoS ONE·2014·129 cit.·DOI

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