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1 with autologous dendritic cells pulsed with Id protein.
2 : muscle regulatory factors, E proteins, and Id proteins.
3 y another class of HLH proteins known as the Id proteins.
4 dependency on the unlimited availability of Id proteins.
5 el transcriptional activity of the mammalian Id proteins.
6 eins MyoD and E12, and not at all with other Id proteins.
7 ele, leading to an overall reduced dosage of Id proteins.
8 n emphasis on the known requirements for the ID proteins.
9 sarcomas coordinately overexpressed USP1 and ID proteins.
10 ergistic activity of Gata4 and Nkx2.5 by the Id proteins.
11 characteristic of intrinsically disordered (ID) proteins.
16 dritic cells (DCs) pulsed with tumor-derived Id protein and now report on 35 patients treated using t
17 indicating that myeloma cells could process Id protein and present Id peptides in the context of the
18 Myozap is a recent addition to the list of ID proteins and has been implicated in serum-response fa
19 he G1 progression and apoptosis functions of Id proteins and hint at a common mechanism for this fami
22 responses, suggesting a mechanism involving Id protein- and E protein-mediated survival and differen
37 ng near a specific set of 170 genes encoding ID proteins are significantly enriched for association w
40 hibitors of differentiation and DNA binding (Id) proteins are known to negatively regulate many bHLH
41 es encoding cardiomyocyte intercalated disc (ID) proteins are more enriched for associations with QT
44 , including modulation of DNA binding by the Id proteins, association with the transcriptional modula
45 th adaptive and innate-like requirements for ID proteins at distinct checkpoints during iNKT cell dev
46 en receptor and/or cytokine signaling, the E-Id protein axis modulates the activities of the PI3K-AKT
47 It is now well established that the E and Id protein axis regulates multiple steps in lymphocyte d
48 previous observations, we propose that the E-Id protein axis specifies innate and adaptive lymphoid c
54 ctivities of E proteins and their antagonist Id proteins, but how these factors regulate early T cell
56 s effector RBPSuh (CSL), GATA-3, E2A/HEB and Id proteins, c-Myb, TCF-1, and members of the Runx, Ets,
57 NA-binding domain, all four of the mammalian Id proteins can activate GAL4-dependent transcription.
59 ants and in vivo overexpression to show that Id proteins can differentially inhibit the activities of
61 Inhibitor of differentiation/DNA binding (Id) proteins comprise a class of helix-loop-helix transc
64 n factors and their negative regulators, the Id proteins, control the development of iNKT sublineages
65 E proteins and their natural inhibitors, the Id proteins, control the timing of differentiation and t
71 knockdown in osteosarcoma cells precipitated ID protein destabilization, cell-cycle arrest, and osteo
72 nisms that control the balance between E and Id proteins during DC subset specification remain unknow
74 of lineage-specific transcription factors by Id proteins enables the self-renewal response to LIF/STA
76 in myoblasts (a) decreased the level of the Id proteins, even in a culture in growth medium, and (b)
78 ins to activate them, with expression of the Id protein Extramacrochaetae (Emc), which antagonizes bH
79 ifier screen in Drosophila, we show that the Id protein Extramacrochaetae enables growth by suppressi
85 ific immune response detecting tumor-derived Id proteins from the original tumor and from all tumor v
91 ese studies show that the entire ensemble of Id proteins has the ability to interact with E47, identi
92 esults are consistent with the idea that the Id proteins have a transcriptional activity when present
93 s a "hot spot" for heart disease, as several ID proteins have been found mutated in cardiomyopathy.
96 bers of the helix-loop-helix (HLH) family of Id proteins have demonstrated roles in the regulation of
98 oteins and their functional antagonists, the ID proteins, have significant roles in normal hematopoie
99 in clinical studies of Id vaccination using Id proteins.However, Id protein is laborious and time-co
104 consequence of (i) binding and sequestering Id proteins, (ii) accelerating their ubiquitination and
105 quamous cell carcinoma of the head and neck, Id protein immunoreactivity was observed in the majority
106 nd in knockout mice implicate E proteins and ID proteins in a wide variety of diseases, belying the n
108 ht to determine the functional role of these Id proteins in BMP-induced osteoblast differentiation.
110 We found that lentiviral overexpression of ID proteins in cord blood HSCs biases myeloerythroid com
112 steroid hormone receptors in particular and ID proteins in general can have multiple functionally di
116 s directly interact with previously reported ID proteins in six known pathways essential for cognitiv
117 stem cells is the constitutive expression of ID proteins in the former and inducible expression in th
118 oteasomes, and (iii) decreasing the level of Id proteins in the nucleus by increasing their transloca
121 tablished that inhibitor of differentiation (Id) proteins, including Id1, Id2, and Id3, associate wit
124 ous or ectopic inhibitor of differentiation (Id) proteins inhibited the differentiation of P19 cells
125 ression in mesenchymal stem cells stabilized ID proteins, inhibited osteoblastic differentiation, and
126 of Id vaccination using Id proteins.However, Id protein is laborious and time-consuming to produce.
127 ion of the Id-specific memory B cells by the Id protein is largely independent of the FcgammaRIIB and
130 transcription factors and their inhibitors, Id proteins, is important for the myeloid-versus-lymphoi
132 s and suggest that deregulated expression of Id proteins may be an epigenetic mechanism to silence ex
134 on of protein-protein interactions involving ID proteins may therefore be possible through the target
136 ture and myelinating oligodendrocytes via an ID protein-mediated negative regulation and may serve as
143 dium, and (b) overcame the inhibition by the Id proteins of MyoD- and E47 dependent transcription and
144 ition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vit
145 ulated that demonstrates dominant effects of Id proteins on different aspects of cellular growth.
148 uctural features underlying the functions of ID proteins/peptides by conventional methods, such as X-
156 iption factors and their natural inhibitors, Id proteins, play critical and complex roles during lymp
160 how the folding of intrinsically disordered (ID) protein sequences, in particular, and population shi
163 at the deubiquitinating enzyme USP1 promotes ID protein stability and stem cell-like characteristics
164 eterodimers in a manner similar to MISTI and Id proteins, suggesting a possible transcriptional inhib
165 an inhibitor of differentiation/DNA binding (Id) proteins that comprise a class of helix-loop-helix f
167 plained experimental observations related to Id proteins; the speed of response varies with the initi
169 , we explore relationships of E proteins and ID proteins to a variety of disease processes and highli
170 ese activities are related to the ability of Id proteins to antagonize E proteins and other transcrip
171 on can be functionally replaced by fusion of Id proteins to SAP-1, whereby the Id moiety then acts to
173 y expressed E2A or inhibitor of DNA binding (Id) proteins to activate or inhibit transcription, respe
174 pression levels of Inhibitor of DNA binding (ID) proteins to ask whether lineage priming affects self
176 e demonstrated a potent inhibitory effect of ID proteins upon CLOCK-BMAL1 transactivation of clock ge
179 ection than a traditional lymphoma idiotype (Id) protein vaccine, and in combination with chemotherap
182 s expressed in T-BET(+) NKT1 cells, and both Id proteins were required for the formation of this subl
184 ther ILCs, iNKT cells constitutively express ID proteins, which antagonize the E protein transcriptio
185 Studies involving ectopic expression of Id proteins, which inhibit E2A as well as other basic he
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