Ask about this productRelated genes to: DRAM antibody
- Gene:
- DRAM1 NIH gene
- Name:
- DNA damage regulated autophagy modulator 1
- Previous symbol:
- -
- Synonyms:
- FLJ11259, DRAM
- Chromosome:
- 12q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2009-06-12
- Date modifiied:
- 2017-03-22
- Gene:
- TMEM150B NIH gene
- Name:
- transmembrane protein 150B
- Previous symbol:
- TMEM224
- Synonyms:
- TTN2, DRAM3
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2009-02-24
- Date modifiied:
- 2019-04-17
Related products to: DRAM antibody
Related articles to: DRAM antibody
- Macroautophagy (hereafter referred to as autophagy) is controlled by a number of core proteins that are critical for all autophagy responses. In addition, a number of autophagy regulators have been found that are not critical for macroautophagy per se, but which play roles in regulating autophagy in either selective situations or in response to specific stimuli. In a recent study, we reported the initial characterization of a new autophagy regulator encoded by TMEM150B that is related to the Damage-Regulated Autophagy Modulator, DRAM1. We have termed this factor DRAM3 for DRAM-Related/Associated Member 3. Interestingly, like DRAM1, DRAM3 regulates both autophagy and cell death, but we found these two functions of the protein are not intrinsically connected. - Source: PubMed
Mrschtik MichaelaRyan Kevin M - Macroautophagy is a membrane-trafficking process that delivers cytoplasmic constituents to lysosomes for degradation. The process operates under basal conditions as a mechanism to turnover damaged or misfolded proteins and organelles. As a result, it has a major role in preserving cellular integrity and viability. In addition to this basal function, macroautophagy can also be modulated in response to various forms of cellular stress, and the rate and cargoes of macroautophagy can be tailored to facilitate appropriate cellular responses in particular situations. The macroautophagy machinery is regulated by a group of evolutionarily conserved autophagy-related (ATG) proteins and by several other autophagy regulators, which either have tissue-restricted expression or operate in specific contexts. We report here the characterization of a novel autophagy regulator that we have termed DRAM-3 due to its significant homology to damage-regulated autophagy modulator (DRAM-1). DRAM-3 is expressed in a broad spectrum of normal tissues and tumor cells, but different from DRAM-1, DRAM-3 is not induced by p53 or DNA-damaging agents. Immunofluorescence studies revealed that DRAM-3 localizes to lysosomes/autolysosomes, endosomes and the plasma membrane, but not the endoplasmic reticulum, phagophores, autophagosomes or Golgi, indicating significant overlap with DRAM-1 localization and with organelles associated with macroautophagy. In this regard, we further proceed to show that DRAM-3 expression causes accumulation of autophagosomes under basal conditions and enhances autophagic flux. Reciprocally, CRISPR/Cas9-mediated disruption of DRAM-3 impairs autophagic flux confirming that DRAM-3 is a modulator of macroautophagy. As macroautophagy can be cytoprotective under starvation conditions, we also tested whether DRAM-3 could promote survival on nutrient deprivation. This revealed that DRAM-3 can repress cell death and promote long-term clonogenic survival of cells grown in the absence of glucose. Interestingly, however, this effect is macroautophagy-independent. In summary, these findings constitute the primary characterization of DRAM-3 as a modulator of both macroautophagy and cell survival under starvation conditions. - Source: PubMed
Publication date: 2015/05/01
Mrschtik MO'Prey JLao L YLong J SBeaumatin FStrachan DO'Prey MSkommer JRyan K M