نتایج جستجو برای: روش mad

تعداد نتایج: 373276  

Journal: :Genetics 1995
J J Sekelsky S J Newfeld L A Raftery E H Chartoff W M Gelbart

The decapentaplegic (dpp) gene of Drosophila melanogaster encodes a growth factor that belongs to the transforming growth factor-beta (TGF-beta) superfamily and that plays a central role in multiple cell-cell signaling events throughout development. Through genetic screens we are seeking to identify other functions that act upstream, downstream or in concert with dpp to mediate its signaling ro...

Journal: :Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 1995
P J Koskinen D E Ayer R N Eisenman

Mad is a bHLH/Zip protein that, as a heterodimer with Max, can repress Myc-induced transcriptional transactivation. Expression of Mad is induced upon terminal differentiation of several cell types, where it has been postulated to down-regulate Myc-induced genes that drive cell proliferation. Here we show that Mad also blocks transformation of primary rat embryo fibroblasts by c-Myc and the acti...

Journal: :Development 1998
R G Wisotzkey A Mehra D J Sutherland L L Dobens X Liu C Dohrmann L Attisano L A Raftery

Mothers against dpp (Mad) mediates Decapentaplegic (DPP) signaling throughout Drosophila development. Here we demonstrate that Medea encodes a MAD-related protein that functions in DPP signaling. MEDEA is most similar to mammalian Smad4 and forms heteromeric complexes with MAD. Like dpp, Medea is essential for embryonic dorsal/ventral patterning. However, Mad is essential in the germline for oo...

2009
Carlos Merino Jay Penney Miranda González Kazuya Tsurudome Myriam Moujahidine Michael B. O'Connor Esther M. Verheyen Pejmun Haghighi

Bone morphogenic protein (BMP) signaling is essential for the coordinated assembly of the synapse, but we know little about how BMP signaling is modulated in neurons. Our findings indicate that the Nemo (Nmo) kinase modulates BMP signaling in motor neurons. nmo mutants show synaptic structural defects at the Drosophila melanogaster larval neuromuscular junction, and providing Nmo in motor neuro...

2004
Jia Tang

In this paper, we propose multi-antenna diversity (MAD), a new transmit diversity scheme for wireless communications. Specifically, MAD selects the optimal transmit antenna with the best channel quality to send data. Due to its greatly simplified architecture, MAD guarantees the simple decoding without imposing any constraints on the issues such as code delay, code rate, antenna number, and mod...

2004
MENACHEM KOJMAN

For an infinite cardinal μ, MAD(μ) denotes the set of all cardinalities of nontrivial maximal almost disjoint families over μ. Erdős and Hechler proved in [7] the consistency of μ ∈ MAD(μ) for a singular cardinal μ and asked if it was ever possible for a singular μ that μ / ∈ MAD(μ), and also whether 2 μ < μ =⇒ μ ∈ MAD(μ) for every singular cardinal μ. We introduce a new method for controlling ...

2016
Linda D. Sharples Abigail L. Clutterbuck-James Matthew J. Glover Maxine S. Bennett Rebecca Chadwick Marcus A. Pittman Timothy G. Quinnell

Obstructive sleep apnoea-hypopnoea (OSAH) causes excessive daytime sleepiness, impairs quality-of-life, and increases cardiovascular disease and road traffic accident risks. Continuous positive airway pressure (CPAP) treatment and mandibular advancement devices (MAD) have been shown to be effective in individual trials but their effectiveness particularly relative to disease severity is unclear...

Journal: :The Quality Assurance Journal 2006

Journal: :Development 1997
S J Newfeld A Mehra M A Singer J L Wrana L Attisano W M Gelbart

Mothers against dpp (Mad) is the prototype of a family of genes required for signaling by TGF-beta related ligands. In Drosophila, Mad is specifically required in cells responding to Decapentaplegic (DPP) signals. We further specify the role of Mad in DPP-mediated signaling by utilizing tkvQ199D, an activated form of the DPP type I receptor serine-threonine kinase thick veins (tkv). In the embr...

2014
Mark W. Moyle Taekyung Kim Neil Hattersley Julien Espeut Dhanya K. Cheerambathur Karen Oegema Arshad Desai

Recruitment of Mad1-Mad2 complexes to unattached kinetochores is a central event in spindle checkpoint signaling. Despite its importance, the mechanism that recruits Mad1-Mad2 to kinetochores is unclear. In this paper, we show that MAD-1 interacts with BUB-1 in Caenorhabditis elegans. Mutagenesis identified specific residues in a segment of the MAD-1 coiled coil that mediate the BUB-1 interacti...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید