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Lc3b 1

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LC3B-I is a cellular protein marker that is involved in the process of autophagy, a fundamental cellular process by which damaged or unwanted components are recycled. It serves as a reliable indicator of the initiation of autophagy within cells.

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Lab products found in correlation

Lc3b 2, by Cell Signaling Technology (5 mentions) Caspase 3, by Cell Signaling Technology (2 mentions) Gapdh, by Cell Signaling Technology (2 mentions) Bcl 2, by Cell Signaling Technology (2 mentions) 4 6 diamidino 2 phenylindole (dapi), by Thermo Fisher Scientific (2 mentions) Atg12, by Cell Signaling Technology (1 mentions) Cell counting kit 8 cck 8, by Dojindo Laboratories (1 mentions) N acetyl l cysteine nac, by Merck Group (1 mentions) Phospho jnk, by Cell Signaling Technology (1 mentions) Phospho p38, by Cell Signaling Technology (1 mentions) Poly adp ribose polymerase, by Cell Signaling Technology (1 mentions) Atg 12 atg 5, by Cell Signaling Technology (1 mentions) Caspase 7, by Cell Signaling Technology (1 mentions) P erk, by Cell Signaling Technology (1 mentions) Dimethyl sulfoxide (dmso), by Merck Group (1 mentions) Nupage lds sample buffer 4, by Thermo Fisher Scientific (1 mentions) Protein sample loading buffer, by LI COR (1 mentions) Pampkα1 α2, by Cell Signaling Technology (1 mentions) Goat anti rabbit ir 800 and goat anti mouse ir 680 antibodies, by LI COR (1 mentions) Western blot gels, by Thermo Fisher Scientific (1 mentions)

Close spelling variants of this product

Anti-LC3B-I/II

5 protocols using lc3b 1

1

Quantifying Autophagy Markers in Cells

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The primary antibodies directed at LC3B-I and LC3B-II were obtained from Cell Signaling (Beverly, MA); the primary antibody directed at GADPH was obtained from Abcam (Cambridge, MA); the secondary antibodies were obtained from Santa Cruz Biotechnology (Santa Cruz, CA). Unless otherwise stated, all other chemicals were obtained from Sigma-Aldrich (St. Louis, MO).
Kikuchi S., Piraino G., O'Connor M., Wolfe V., Ridings K., Lahni P, & Zingarelli B. (2020). Hepatocyte-Specific Deletion of AMPKα1 Results in Worse Outcomes in Mice Subjected to Sepsis in a Sex-Specific Manner. Frontiers in Immunology, 11, 210.
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2

Polyphyllin VI Induces Autophagy and Apoptosis

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Purified Polyphyllin VI (>98%) was purchased from Chengdu Must Bio-Technology Co., Ltd (Chengdu, China). Stock solution was dissolved in DMSO (Sigma, St. Louis, MO, USA) and was stored in the dark at −20°C. Then, the diluting stock solution was diluted into working concentrations by culture medium immediately before use. CCK8 (Cell Counting Kit-8) was purchased from Dojindo Molecular Technologies, Inc (Japan). N-acetyl-L-cysteine (NAC) was purchased from Sigma Chemical Co. (St. Louis, MO, USA). Antibodies against poly ADP-ribose polymerase (PARP), Bax, Bcl-2, LC3B-I, LC3B-II, p62, Atg-7, Atg-5, Atg-12-Atg-5, Atg-12, Atg-3, JNK, phospho-JNK, p38, phospho-p38, p-ERK, ERK, caspase-3, caspase-7, and GAPDH were purchased from Cell Signaling Technology (Beverly, MA, USA).
Yuan Y.L., Jiang N., Li Z.Y., Song Z.Z., Yang Z.H., Xue W.H., Zhang X.J, & Du Y. (2019). Polyphyllin VI induces apoptosis and autophagy in human osteosarcoma cells by modulation of ROS/JNK activation. Drug Design, Development and Therapy, 13, 3091-3103.
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3

AICAR Signaling Pathway Analysis

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The AMP analog, AICAR, was obtained from LC Laboratories (Woburn, MA). Primary antibodies for AMPKα1/α2, pAMPKα1/α2, and LC3B-I and LC3B-II were obtained from Cell Signaling Technology (Danvers, MA). Primary antibodies for GAPDH and for PGC1-α were obtained from Abcam (Cambridge, MA). The Odyssey blocking buffer, LI-COR goat anti-rabbit IR-800 and goat anti-mouse IR-680 antibodies, and the 4× Protein Sample Loading Buffer were obtained from LI-COR Biotechnology (Lincoln, NE). The NuPAGE® LDS Sample Buffer (4×), and Western blot gels were purchased from Life Technologies (Grand Island, NY). All other chemicals were obtained from Sigma-Aldrich (St. Louis, MO).
Matsiukevich D., Piraino G., Klingbeil L.R., Hake P.W., Wolfe V., O’Connor M, & Zingarelli B. (2017). THE AMPK ACTIVATOR AICAR AMELIORATES AGE-DEPENDENT MYOCARDIAL INJURY IN MURINE HEMORRHAGIC SHOCK. Shock (Augusta, Ga.), 47(1), 70-78.
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4

AMPK Activation and Autophagy Regulation

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The AMPK activator A769662 was obtained from LC Laboratories (Woburn, Mass). The primary antibodies directed at AMPKα1/2, pAMPKα1/2, AMPK β1/2, pAMPKβ1, LC3B-I, and LC3B-II were obtained from Cell Signaling (Beverly, Mass); the primary antibody directed at PGC-1α, was obtained from Abcam (Cambridge, Mass). The primary antibodies directed at SIRT1 and β-actin and the secondary antibodies were obtained from Santa Cruz Biotechnology (Santa Cruz, Calif). The Odyssey blocking and loading buffers and LI-COR secondary antibodies were obtained from LI-COR Biotechnology (Lincoln, Nebr). All other chemicals were obtained from Sigma-Aldrich (St. Louis, Mo).
Kitzmiller L., Ledford J.R., Hake P.W., O'Connor M., Piraino G, & Zingarelli B. (2019). Activation of AMP-Activated Protein Kinase by A769662 Ameliorates Sepsis-Induced Acute Lung Injury in Adult Mice. Shock (Augusta, Ga.), 52(5).
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5

Apoptosis and Autophagy Evaluation

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Cantharidin was purchased from Sigma. Propidium iodide (PI) and DAPI (dihydrochloride) were purchased from Thermo Fisher Scientific. PARP, cleaved PARP, caspase 3, cleaved caspase 3, Bax, Bcl-2, LC3B I, LC3B II, p62, Beclin-1, and GAPDH antibodies were purchased from Cell Signaling Technology (MA, USA)
Li H.C., Xia Z.H., Chen Y.F., Yang F., Feng W., Cai H., Mei Y., Jiang Y.M., Xu K, & Feng D.X. (2017). Cantharidin Inhibits the Growth of Triple-Negative Breast Cancer Cells by Suppressing Autophagy and Inducing Apoptosis in Vitro and in Vivo. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 43(5).
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