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Rabbit Anti-MAP1LC3C Recombinant Antibody (D1R8V) (CBMAB-CP1362-LY)

The product is antibody recognizes MAP1LC3C. The antibody D1R8V immunoassay techniques such as: WB.
See all MAP1LC3C antibodies

Summary

Host Animal
Rabbit
Specificity
Human
Clone
D1R8V
Antibody Isotype
IgG
Application
WB

Basic Information

Immunogen
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu50 of human LC3C protein.
Specificity
Human
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
100 µg/ml BSA, 50% glycerol
Preservative
0.02% sodium azide
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Microtubule Associated Protein 1 Light Chain 3 Gamma
Introduction
Autophagy is a highly regulated bulk degradation process that plays an important role in cellular maintenance and development. MAP1LC3C is an ortholog of the yeast autophagosome protein Atg8 (He et al., 2003 [PubMed 12740394]).[supplied by OMIM, Nov 2010]
Entrez Gene ID
440738
UniProt ID
Q9BXW4
Alternative Names
Microtubule Associated Protein 1 Light Chain 3 Gamma; Autophagy-Related Ubiquitin-Like Modifier LC3 C; MAP1 Light Chain 3-Like Protein 3; Autophagy-Related Protein LC3 C; MAP1A/MAP1B Light Chain 3 C; MAP1A/MAP1B LC3 C; Microtubule-Associated Proteins 1A/1B Light Chain 3C;
Function
Ubiquitin-like modifier that plays a crucial role in antibacterial autophagy (xenophagy) through the selective binding of CALCOCO2 (PubMed:23022382).
Recruits all ATG8 family members to infecting bacteria such as S.typhimurium (PubMed:23022382).
May also play a role in aggrephagy, the macroautophagic degradation of ubiquitinated and aggregated proteins (PubMed:28404643).
Biological Process
AggrephagyManual Assertion Based On ExperimentIMP:UniProtKB
Autophagosome assemblyManual Assertion Based On ExperimentIBA:GO_Central
Autophagosome maturationManual Assertion Based On ExperimentIDA:UniProtKB
Autophagy of mitochondrionManual Assertion Based On ExperimentIBA:GO_Central
Cellular response to nitrogen starvationManual Assertion Based On ExperimentIBA:GO_Central
Cellular response to starvationManual Assertion Based On ExperimentIDA:UniProtKB
MacroautophagyManual Assertion Based On ExperimentIDA:UniProtKB
Protein exit from endoplasmic reticulumManual Assertion Based On ExperimentIMP:CACAO
Cellular Location
Cytoplasmic vesicle, autophagosome membrane
Endomembrane system
Cytoplasm, cytoskeleton
LC3-II binds to the autophagic membranes.
PTM
The precursor molecule is cleaved by ATG4 (ATG4A, ATG4B, ATG4C or ATG4D) to expose the glycine at the C-terminus and form the cytosolic form, LC3-I (PubMed:15187094, PubMed:20818167, PubMed:30661429, PubMed:31709703).
The processed form is then activated by APG7L/ATG7, transferred to ATG3 and conjugated to phosphatidylethanolamine (PE) phospholipid to form the membrane-bound form, LC3-II (PubMed:15187094).
During non-canonical autophagy, the processed form is conjugated to phosphatidylserine (PS) phospholipid (PubMed:33909989).
ATG4 proteins also mediate the delipidation of PE-conjugated forms (PubMed:33909989, PubMed:31709703).
In addition, ATG4B and ATG4D mediate delipidation of ATG8 proteins conjugated to PS during non-canonical autophagy (PubMed:33909989).
(Microbial infection) The Legionella effector RavZ is a deconjugating enzyme that hydrolyzes the amide bond between the C-terminal glycine residue and an adjacent aromatic residue in ATG8 proteins conjugated to phosphatidylethanolamine (PE), producing an ATG8 protein that is resistant to reconjugation by the host machinery due to the cleavage of the reactive C-terminal glycine (PubMed:23112293, PubMed:31722778).
RavZ is also able to mediate delipidation of ATG8 proteins conjugated to phosphatidylserine (PS) (PubMed:33909989).
Phosphorylation at Ser-96 and Ser-98 by TBK1 prevents interaction with ATG4 (ATG4A, ATG4B, ATG4C or ATG4D) (PubMed:31709703).
Phosphorylation by TBK1 on autophagosomes prevents their delipidation by ATG4 and premature removal from nascent autophagosomes (PubMed:31709703).

Verma, R., Aggarwal, P., Bischoff, M. E., Reigle, J., Secic, D., Wetzel, C., ... & Czyzyk-Krzeska, M. F. (2023). Microtubule-associated protein MAP1LC3C regulates lysosomal exocytosis and induces zinc reprogramming in renal cancer cells. Journal of Biological Chemistry, 299(5).

Zhang, X., Li, K., Zhong, S., Liu, S., Liu, T., Li, L., ... & Bao, Y. (2022). Immunotherapeutic Value of MAP1LC3C and Its Candidate FDA-Approved Drugs Identified by Pan-Cancer Analysis, Virtual Screening and Sensitivity Analysis. Frontiers in Pharmacology, 13, 863856.

Qi, L., Sun, B., Yang, B., & Lu, S. (2022). PGM5P3-AS1 regulates MAP1LC3C to promote cell ferroptosis and thus inhibiting the malignant progression of triple-negative breast cancer. Breast Cancer Research and Treatment, 193(2), 305-318.

Verma, R., Aggarwal, P., Reigle, J., Secic, D., Wetzel, C., Bischoff, M. E., ... & Czyzyk-Krzeska, M. F. (2022). MAP1LC3C regulates lysosomal exocytosis and induces zinc reprogramming in renal cancer cells. bioRxiv, 2022-05.

Bischoff, M. E., Zang, Y., Chu, J., Price, A. D., Ehmer, B., Talbot, N. J., ... & Czyzyk-Krzeska, M. F. (2021). Selective MAP1LC3C (LC3C) autophagy requires noncanonical regulators and the C-terminal peptide. Journal of Cell Biology, 220(7), e202004182.

Cho, H. S., Park, S. Y., Kim, S. M., Kim, W. J., & Jung, J. Y. (2021). Autophagy-related protein MAP1LC3C plays a crucial role in odontogenic differentiation of human dental pulp cells. Tissue Engineering and Regenerative Medicine, 18, 265-277.

Bischoff, M. E., Zang, Y., Chou, J., Price, A. D., Ehmer, B., Talbot, N. J., ... & Czyzyk-Krzeska, M. F. (2021). Selective MAP1LC3C (LC3C) autophagy requires noncanonical initiation regulators and the paralog-specific C-terminal peptide. bioRxiv, 2021-02.

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For research use only. Not intended for any clinical use.

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