The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues.

By T. Lindsten, Andrea J. Ross, Ayala King, W. Zong, J. Rathmell, Helena Shiels, E. Ulrich, K. Waymire, Patryce L. Mahar, Kenneth and 14 more. Molecules and Cells, 2000

1,515 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e45cbcbc8d386db9938e13a1c88e341f3bc9f6a9

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Citations in the corpus

• Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 (2014, background): “Conversely, the simultaneous ablation of Bax and Bak1(288) or Bcl2l11 and Bmf (encoding two BH3-only proteins involved in MOMP initiation) truly prevents the programmed demise of several cell types, causing their persistence throughout adult life.(292,293) These observations”
• Ferroptosis: Death by Lipid Peroxidation. (2016, background): “By analogy, the limbs of mice lacking Bak develop normally, whereas mice lacking both Bax and Bak fail to achieve a sufficient level of physiological cell death and display persistent interdigital webbing [50].”
• The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “, 2001) and dramatically impairs developmentally programmed attrition in several tissues (Lindsten et al., 2000), typically resulting in perinatal death.”
• Programmed Cell Death in Animal Development and Disease (2011, positive): “Perhaps the best-known example is the formation of digits in higher vertebrates in which PCD eliminates the interdigital webs primarily via the apoptotic machinery (Figure 2A; Lindsten et al., 2000).”
• Programmed cell senescence during mammalian embryonic development. (2013, neutral): “In relation to this, for example, severe disabling of apoptosis results in relatively minor developmental defects, restricted to imperforate vaginas and a partial persistence of interdigital webs (Lindsten et al., 2000; Ren et al., 2010).”
• Ways of dying: multiple pathways to apoptosis. (2003, background): “Both pro-apoptotic factions seem to be required for launching apoptosis: the damage-sensing BH3-only proteins primarily antagonize the Bcl-2like proteins (Huang and Strasser 2000), whereas either Bax or Bak is essential downstream, probably in organelle perturbation (Lindsten et al. 2000; Cheng et a”
• Alkylating DNA damage stimulates a regulated form of necrotic cell death. (2004, background): “…lacking both Bax and Bak are resistant to apoptosis induced by developmental cues, signal transduction through death receptors, growth factor withdrawal, and ER stress (Lindsten et al. 2000; Cheng et al. 2001; Wei et al. 2001; Zong et al. 2001, 2003; Degenhardt et al. 2002b; Scorrano et al. 2003).”
• Control of mitochondrial apoptosis by the Bcl-2 family (2009, background): “Apoptosis that is caused by BH3-only proteins absolutely requires Bax and Bak (Kuwana et al., 2005; Lindsten et al., 2000; Wei et al., 2000; Wei et al., 2001).”
• Apo2L/TRAIL: apoptosis signaling, biology, and potential for cancer therapy. (2003, background): “[43] Lindsten T, Ross AJ, King A, Zong WX, Rathmell JC, Shiels HA, et al.”
• Keeping killers on a tight leash: transcriptional and post-translational control of the pro-apoptotic activity of BH3-only proteins (2002, background): “persistence of interdigitating webbing and progressive lymphadenopathy.(28) Intriguingly, the lymphoid phenotype of baxbak mice(28) is remarkably similar to that caused by Bim-deficiency,(23) indicating that Bim and Bax/Bak might act in the same pathway.”
• Apo2L/TRAIL and its death and decoy receptors (2003, background): “outs of Bax and Bak, thymocytes remain sensitive to Fas despite the inactivation of the intrinsic pathway.(41) Type II cells, on the other hand, cannot die in response to Fas”
• How do BCL-2 proteins induce mitochondrial outer membrane permeabilization? (2008, positive): “The direct activation of BAX and BAK model The effector molecules BAX and BAK are essential for MOMP, because combined deletion renders cells resistant to multiple pro-apoptotic stimulation [29, 30 ].”