R
Rivka Ofir
Researcher at Ben-Gurion University of the Negev
Publications - 92
Citations - 3317
Rivka Ofir is an academic researcher from Ben-Gurion University of the Negev. The author has contributed to research in topics: Gene & Phosphorylation. The author has an hindex of 31, co-authored 87 publications receiving 2993 citations. Previous affiliations of Rivka Ofir include Salk Institute for Biological Studies & National Institute of Biotechnology.
Papers
More filters
Journal ArticleDOI
Negative and positive regulation by transcription factor cAMP response element-binding protein is modulated by phosphorylation.
TL;DR: CREB has a dual function, that of a repressor in the absence of phosphorylation and an activator when phosphorylated by protein kinase A.
Journal ArticleDOI
Citral is a new inducer of caspase-3 in tumor cell lines.
TL;DR: Concentrations of 44.5 muM, comparable to the concentration of citral in a cup of tea prepared from 1 g of lemon grass, induced apoptosis in several hematopoietic cancer cell lines, accompanied by DNA fragmentation and caspase-3 catalytic activity induction.
Journal ArticleDOI
PLA2G6 Mutation Underlies Infantile Neuroaxonal Dystrophy
Shareef Khateeb,Hagit Flusser,Rivka Ofir,Ilan Shelef,Ginat Narkis,Gideon Vardi,Zamir Shorer,Rachel Levy,Aharon Galil,Khalil Elbedour,Ohad S. Birk +10 more
TL;DR: Findings highlight a role of phospholipase in neurodegenerative disorders and identify an underlying mutation common to both affected families in PLA2G6, the gene encoding phospholIPase A2 group VI (cytosolic, calcium-independent).
Journal ArticleDOI
Maternally inherited Birk Barel mental retardation dysmorphism syndrome caused by a mutation in the genomically imprinted potassium channel KCNK9.
Ortal Barel,Stavit A. Shalev,Rivka Ofir,Asi Cohen,Joël Zlotogora,Zamir Shorer,Galia Mazor,Gal Finer,Shareef Khateeb,Noam Zilberberg,Ohad S. Birk,Ohad S. Birk +11 more
TL;DR: A maternally transmitted genomic-imprinting syndrome of mental retardation, hypotonia, and unique dysmorphism with elongated face is described and it is demonstrated that the disease is caused by a missense mutation in the maternal copy of KCNK9 within this locus.
Journal ArticleDOI
Phosphorylation of the C terminus of Fos protein is required for transcriptional transrepression of the c-fos promoter
TL;DR: In this paper, it was shown that mutant c-Fos protein which is hypophosphorv lated at its C terminus is unable to repress transcription of the c-fos promoter following induction with serum or tetraphorbol acetate.