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ATP5G1

Official Full Name
ATP synthase, H+ transporting, mitochondrial Fo complex, subunit C1 (subunit 9)
Background
This gene encodes a subunit of mitochondrial ATP synthase. Mitochondrial ATP synthase catalyzes ATP synthesis, utilizing an electrochemical gradient of protons across the inner membrane during oxidative phosphorylation. ATP synthase is composed of two linked multi-subunit complexes: the soluble catalytic core, F1, and the membrane-spanning component, Fo, comprising the proton channel. The catalytic portion of mitochondrial ATP synthase consists of 5 different subunits (alpha, beta, gamma, delta, and epsilon) assembled with a stoichiometry of 3 alpha, 3 beta, and a single representative of the other 3. The proton channel seems to have nine subunits (a, b, c, d, e, f, g, F6 and 8). This gene is one of three genes that encode subunit c of the proton channel. Each of the three genes have distinct mitochondrial import sequences but encode the identical mature protein. Alternatively spliced transcript variants encoding the same protein have been identified.
Synonyms
ATP5G1; ATP synthase, H+ transporting, mitochondrial Fo complex, subunit C1 (subunit 9); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit c (subunit 9), isoform 1 , ATP synthase, H+ transporting, mitochondrial F0 complex, subunit C1 (subunit 9) , ATP5G; ATP synthase lipid-binding protein, mitochondrial; ATP synthase lipid binding protein mitochondrial; ATP synthase proteolipid P1; ATPase protein 9; ATPase subunit C; ATPase subunit 9; OTTHUMP00000218389; OTTHUMP00000218391; OTTHUMP00000218448; OTTHUMP00000218449; OTTHUMP00000218450; mitochondrial ATP synthase, sub; ATP5A; ATP5G; mitochondrial ATP synthase, subunit 9, isoform 1; mitochondrial ATP synthase, subunit C, isoform 1; ATP synthase, H+ transporting, mitochondrial F0 complex, subunit C1 (subunit 9); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit c (subunit 9), isoform 1; zgc:73293; zgc:86684; wu:fb13h01; wu:fb14d03

P1A and Mastocytoma Growth

Gene P1A (P1CTL),a mouse cancer-germline gene encoding a tumor antigen that represents the best mouse model for human MAGE-type tumor antigens, and encodes the major tumor rejection antigen of mastocytoma P815 which is composed of a peptide (LPYLGWLVF, P1A35–43) derived from the P1A protein and presented to cytotoxic T lymphocytes (CTL) by MHC class I molecule H-2 Ld. P1A is activated in several tumors but silent in normal cells except in placental trophoblasts and male germline cells, and these cells do not bear surface MHC class I molecules. They do not present the P1A peptide, so antigen P815A is strictly tumor-specific, and immunization against this peptide does not induce autoimmune side-effects. According to Gaëlle Vandermeulen’ studies, immunization with a plasmid coding for the full-length P1A significantly delayed tumor growth, mice failed to reject tumor and even delay tumor growth.

P1A And Photodynamic Therapy

Photodynamic therapy (PDT) is a two-step procedure which involves the administration of a photosensitizing drug followed by activation of the drug with nonthermal light of a specific wavelength. PDT is thought to be particularly effective at activating an immune response against a locally treated tumor. Among various tumor antigens discovered to date, P1A is the best-described nonmutated mouse cancer-testis tumor antigen and has been used for many immunotherapy studies, and is expressed in cancers, but not at all or at very low levels in other tissues. In Pawel Mroz et al. Studies, PDT does indeed induce recognition of MHC class I-bound epitope derived from the P1A antigen and provide additional evidence to support the notion that the expression of tumor antigen makes a significant difference in the outcome of PDT.

P1A And Immune Evasion

Tumor evasion of T-cell immunity remains a significant obstacle to adoptive T-cell therapy, but the mode of immune evasion is dictated by the cancer cells or by the tumor antigens. Although P1CTL conferred partial protection, tumors recurred in almost all mice. And the ability of Meth A to cause T-cell death alleviated the need for P1A antigen downregulation in cancer cells.

References:

  1. Gaëlle Vandermeulen, Catherine Uyttenhove, Etienne De Plaen, Benoît J. Van den Eynde and Véronique Préat. (2014) 'Intramuscular electroporation of a P1A-encoding plasmid vaccine delays P815 mastocytoma growth', Bioelectrochemistry, 100:112-118.
  2. Xue-Feng Bai, Jinqing Liu, Ou Li, Pan Zheng and Yang Liu. (2003) 'Antigenic drift as a mechanism for tumor evasion of destruction by cytolytic T lymphocytes', Journal of Clinical Investigation, 111(10):1487–1496.
  3. Xue-Feng Bai, Jin-Qing Liu, Pramod S. Joshi, Lizhong Wang, Lijie Yin, Jadwiga Labanowska, Nyla Heerema, Pan Zheng and Yang Liu. (2006) 'Different Lineages of P1A-Expressing Cancer Cells Use Divergent Modes of Immune Evasion for T-Cell Adoptive Therapy', Cancer Research, 66(16): 8241-9.

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