Abstract: The present disclosure provides mTOR agonists that selectively modulate proteasome dynamics, compositions, methods and uses thereof for modulation of stress-induced proteasome dynamics and related pathological conditions. The present disclosure specifically provides therapeutic methods for treating disorders associated with cytosolic accumulation of the proteasome. The invention further provides prognostic methods for detection and monitoring drug resistant cancers, as well as methods for screening for modulators of proteasome dynamics.

Abstract: The invention provides a method for treating cancer comprising the step of administering a therapeutically effective amount of KPC1, a peptide which is at least about 70% homologous to the KPC1 or an agent which up-regulates KPC1. In some embodiments, there is also provided a method for treating cancer comprising the step of administering a therapeutically effective amount of p50, a peptide which is at least about 70% homologous to the p50 or an agent which up-regulates p50.

Abstract: The invention provides a method for treating cancer comprising the step of administering a therapeutically effective amount of KPC1, a peptide which is at least about 70% homologous to the KPC1 or an agent which up-regulates KPC1. In some embodiments, there is also provided a method for treating cancer comprising the step of administering a therapeutically effective amount of p50, a peptide which is at least about 70% homologous to the p50 or an agent which up-regulates p50.

Abstract: A peptide comprising the amino acid sequence set forth in WILVRLW (SEQ ID NO: 1), or any functionally related variant thereof, a complex, conjugate or chimera comprising the same, wherein the peptide is linked with or without a linker to RING or to a molecule or peptide that recruits E3 ligase and method for treating cancer by administering the same.

Abstract: The invention provides a method for treating cancer comprising the step of administering a therapeutically effective amount of KPC1, a peptide which is at least about 70% homologous to the KPC1 or an agent which up-regulates KPC1. In some embodiments, there is also provided a method for treating cancer comprising the step of administering a therapeutically effective amount of p50, a peptide which is at least about 70% homologous to the p50 or an agent which up-regulates p50.

Abstract: Compositions and methods for modulating the activation of nuclear factor ?B (NF-?B) are provided. The compositions comprise one or more agents that modulate ubiquitination of phosphorylated I?B? and/or I?B?. Such compositions may be used for treating diseases associated with NF-?B activation. Modulating agents include human E3 ubiquitin ligases, antibodies thereto and variants thereof, as well as related proteins.

Abstract: Compositions and methods for modulating the activation of nuclear factor ?B (NF-?B) are provided. The compositions comprise one or more agents that modulate ubiquitination of phosphorylated I?B? and/or I?B? Such compositions may be used for treating diseases associated with NF-?B activation. Modulating agents include human E3 ubiquitin ligases, antibodies thereto and variants thereof, as well as related proteins.

Abstract: The present invention provides novel peptides, nucleic acids, compounds, compositions and methods for regulating apoptosis, and screening methods for identifying same. Regulation of apoptosis is mediated via IAPi-derived proteins, peptide fragments thereof, and nucleic acids encoding same, stimulating/accelerating or downmodulating/suppressing apoptosis. For stimulation/acceleration of apoptosis, the IAPi-derived proteins or peptide fragments thereof comprise RHG and Trp-box amino acid consensus sequences. Stimulation/acceleration results in self-ubiquitination and auto-degradation of an IAP. For downmodulation/suppression of apoptosis, IAPi-derived proteins or peptide fragments thereof comprising either RHG or Trp-box amino acid consensus sequences, or both, failing to stimulate or suppressing self-ubiquitination and auto-degradation of an IAP, result in suppression of apoptosis.

Abstract: Compositions and methods for modulating the activation of nuclear factor ?B (NF-?B) are provided. The compositions comprise one or more agents that modulate ubiquitination of phosphorylated I?B? and/or I?B?. Such compositions may be used for treating diseases associated with NF-?B activation. Modulating agents include human E3 ubiquitin ligases, antibodies thereto and variants thereof, as well as related proteins.

Abstract: Compositions and methods for modulating the activation of nuclear factor ?B (NF-?B) are provided. The compositions comprise one or more agents that modulate ubiquitination of phosphorylated I?B? and/or I?B?. Such compositions may be used for treating diseases associated with NF-?B activation. Modulating agents include human E3 ubiquitin ligases, antibodies thereto and variants thereof, as well as related proteins.

Abstract: Compositions and methods for modulating the activation of nuclear factor ?B (NF-?B) are provided. The compositions comprise one or more agents that modulate ubiquitination of phosphorylated I?B? and/or I?B?. Such compositions may be used for treating diseases associated with NF-?B activation. Modulating agents include human E3 ubiquitin ligases, antibodies thereto and variants thereof, as well as related proteins.

Abstract: The present invention provides novel peptides, nucleic acids, compounds, compositions and methods for regulating apoptosis, and screening methods for identifying same. Regulation of apoptosis is mediated via IAPi-derived proteins, peptide fragments thereof, and nucleic acids encoding same, stimulating/accelerating or downmodulating/suppressing apoptosis. For stimulation/acceleration of apoptosis, the IAPi-derived proteins or peptide fragments thereof comprise RHG and Trp-box amino acid consensus sequences. Stimulation/acceleration results in self-ubiquitination and auto-degradation of an IAP. For downmodulation/suppression of apoptosis, IAPi-derived proteins or peptide fragments thereof comprising either RHG or Trp-box amino acid consensus sequences, or both, failing to stimulate or suppressing self-ubiquitination and auto-degradation of an IAP, result in suppression of apoptosis.

Abstract: The present invention provides novel peptides, nucleic acids, compounds, compositions and methods for regulating apoptosis, and screening methods for identifying same. Regulation of apoptosis is mediated via IAPi-derived proteins, peptide fragments thereof, and nucleic acids encoding same, stimulating/accelerating or downmodulating/suppressing apoptosis. For stimulation/acceleration of apoptosis, the IAPi-derived proteins or peptide fragments thereof comprise RHG and Trp-box amino acid consensus sequences. Stimulation/acceleration results in self-ubiquitination and auto-degradation of an IAP. For downmodulation/suppression of apoptosis, IAPi-derived proteins or peptide fragments thereof comprising either RHG or Trp-box amino acid consensus sequences, or both, failing to stimulate or suppressing self-ubiquitination and auto-degradation of an IAP, result in suppression of apoptosis.

Abstract: The invention discloses anti-tumor activity in the sera of certain reptiles, more particularly in the serum of alligators or crocodiles. The active principle resides in one or more serum proteins or polypeptides that inhibit the growth of mammalian tumor cells in culture while being practically devoid of such inhibitory activity toward normal cells in culture. The active fractions obtained from the sera show no overt toxicity in healthy mammals, and this novel anti-tumor agent may therefore be used for the prevention, investigation, treatment or diagnosis of neoplasms.

Abstract: Compositions and methods for modulating the activation of nuclear factor &kgr;B (NF-&kgr;B) are provided. The compositions comprise one or more agents that modulate ubiquitination of phosphorylated I&kgr;B&agr; and/or I&kgr;B&bgr;. Such compositions may be used for treating diseases associated with NF-&kgr;B activation. Modulating agents include human E3 ubiquitin ligases, antibodies thereto and variants thereof, as well as related proteins.

Abstract: Compositions and methods for modulating the activation of nuclear factor &kgr;B (NF-&kgr;B) are provided. The compositions comprise one or more agents that modulate ubiquitination of phosphorylated I&kgr;B&agr; and/or I&kgr;B&bgr;. Such compositions may be used for treating diseases associated with NF-&kgr;B activation. Modulating agents include human E3 ubiquitin ligases, antibodies thereto and variants thereof, as well as related proteins.

Abstract: Compositions and methods for modulating the activation of nuclear factor &kgr;B (NF-&kgr;B) are provided. The compositions comprise one or more agents that modulate ubiquitination of phosphorylated I&kgr;B&agr; and/or I&kgr;B&bgr;. Such compositions may be used for treating diseases associated with NF-&kgr;B activation. Modulating agents include human E3 ubiquitin ligases, antibodies thereto and variants thereof, as well as related proteins.

Abstract: Compositions and methods for modulating the activation of nuclear factor .kappa.B (NF-.kappa.B) are provided. The compositions comprise one or more agents that modulate ubiquitination of phosphorylated I.kappa.B.alpha. and/or I.kappa.B.beta.. Such compositions may be used for treating diseases associated with NF-.kappa.B activation. Modulating agents include peptides that comprise a recognition domain for E3 ubiquitin ligase.