Publication for Tfap2a and Tfap2b

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression		 CoexViewer
mmu Tfap2a transcription factor AP-2, alpha 21418 [link]
mmu Tfap2b transcription factor AP-2 beta 21419

Pubmed ID Priority Text
28912684 0.98 Tfap2A and Tfap2B are expressed in inhibitory precursors during embryonic development and that their expression persists into adulthood.
0.98 Tfap2A, but not Tfap2B, is capable of inducing the generation of interneurons when misexpressed in the ventricular neuroepithelium.
0.98 Tfap2A and Tfap2B are required for the survival of sympathetic and sensory ganglia progenitors (Schmidt et al.,).
0.98 Tfap2A and Tfap2B have been shown to promote the differentiation of GABAergic and glycinergic amacrine cells (Jin et al.,).
0.98 Tfap2A, but not Tfap2B, has the ability to direct specification of Pax2+ GABAergic interneurons.
0.97 Tfap2A and Tfap2B defines subtypes of GABAergic neurons and plays specific, but complementary roles in the specification of interneurons in the developing cerebellum.
0.97 Tfap2A and Tfap2B in the WM layer of the cerebellum, located superior to the VZ where GABAergic neurons are produced (Figures 1C,D; Hoshino et al.,).
0.97 Tfap2A, but not Tfap2B, is expressed in the PCL (G,I).
0.97 Tfap2A and Tfap2B at E15.5 and P0 supports our earlier observations that Tfap2A and Tfap2B are expressed by GABAergic neurons (Figures 1E-H).
0.97 Tfap2A and Tfap2B indicates that they are expressed as early as E12.5 in the cerebellum when GABAergic neurons are produced, and that their expression persists into adulthood.
0.97 Tfap2A and Tfap2B is restricted to GABAergic neuronal subtypes in the adult cerebellum.
0.97 Tfap2A and Tfap2B are primarily expressed by cells in the VZ and WM (Figures 3D-F).
0.97 Tfap2A and Tfap2B are expressed in GABAergic precursors.
0.97 Tfap2A and Tfap2B expression during this process.
0.97 Tfap2A or Tfap2B are now also expressing Pax2, and that, perhaps, Tfap2A+ and Tfap2B+ cells become GABAergic interneurons expressing Pax2 as they mature in the WM.
0.97 Tfap2A and Tfap2B have independent roles in directing the diversification of cerebellar GABAergic neuronal subtypes in the cerebellum.
0.97 Tfap2B, but not Tfap2A, results in a reduction in Pax2 expression.
0.97 Tfap2A is expressed in all GABAergic neurons, whereas Tfap2B is selectively expressed in the interneuronal population (Figure 2).
0.97 Tfap2A and Tfap2B play independent roles in the specification of GABAergic interneurons during mouse cerebellar development.
0.96 Tfap2A and Tfap2B in the specification of GABAergic neuronal subtypes in mice.
0.96 Tfap2A and Tfap2B transcripts are expressed in the developing and mature mouse cerebellum (Moser et al.,; Shimada et al.,), but the neuronal subtypes within the cerebellum that express these transcription factors have not yet been determined.
0.96 Tfap2B appears to be more widespread than Tfap2A at this stage which may reflect the expression of Tfap2B in non-cerebellar cell types (Figures 1C-F).
0.96 Tfap2A+ and Tfap2B+ cells partake a GABAergic neuron migratory pathway and are expressed by GABAergic precursors in the embryonic cerebellum.
0.96 Tfap2A+ and Tfap2B+ cells in the WM only express Lhx1/5 indicating that they are postmitotic GABAergic neurons (Figures 3G-N).
0.96 Tfap2A and Tfap2B expression precedes Pax2 in the developing cerebellum.
0.96 Tfap2A and Tfap2B precedes the expression of Pax2 and raise the possibility that Tfap2A and Tfap2B regulate the expression of Pax2.
0.96 Tfap2A and Tfap2B in directing the specification of GABAergic neuronal subtypes, we analyzed consequences of misexpressing each transcription factor on the expression of neuronal markers, Pax2, Pax6 and CBP which correspond to GABAergic interneurons, glutamatergic neurons and Purkinje cells, respectively.
0.96 Tfap2B to change the number of Pax2+ interneurons, we found a two-fold increase in the number of Pax2+ interneurons in Tfap2A-misexpressed cells relative to control in the WM (Figures 6A,B,D).
0.96 Tfap2A and Tfap2B defines GABAergic neuronal subtypes and their contribution to the generation and specification of cerebellar GABAergic neurons.
0.96 Tfap2A and Tfap2B. (Ai) In a wild-type, expression of Tfap2A and Tfap2B occur in an overlapping manner in the ventricular zone at E12.5 which is observed superior to Ptf1a territory.
0.96 Tfap2A and Tfap2B may distinguish GABAergic projection neurons from interneurons in the developing cerebellum.
0.95 Tfap2A and Tfap2B have been demonstrated to play important roles for the development of a variety of tissues including the nervous system, kidney, skeleton, skin, limbs and the eye (Schorle et al.,; Zhang et al.,; Nottoli et al.,; West-Mays et al.,; Eckert et al.,; Seberg et al.,).
0.95 Tfap2A and Tfap2B is detected in the underlying WM at E12.5 (C,D) and E15.5 (E,F) where inhibitory neurons transit after exiting the VZ.
0.95 Tfap2A+ cells consist of a subset of Tfap2B+ cells and suggests that their expression defines distinct neuronal subpopulations.
0.94 Tfap2A is expressed by all GABAergic neurons, whereas Tfap2B is selectively expressed by interneurons.
0.94 Tfap2 transcription factors in the development of GABAergic neurons and determine their functional relevance, we analyzed the expression of Tfap2A and Tfap2B in the developing mouse cerebellum.
0.94 Tfap2A and Tfap2B are expressed by mitotic or postmitotic GABAergic neurons, we assessed whether these cells express transcription factors Lhx1/5 (postmitotic), Olig2 and Pax2 (both mitotic and postmitotic; Maricich and Herrup,; Chizhikov et al.,; Morales and Hatten,; Zhao et al.,).
0.94 Tfap2A (E15.5: 97 +- 1%, E18.5: 89 +- 4%) and Tfap2B (E15.5: 88 +- 4%, E18.5: 90 +- 2%) at both E15.5 and E18.5.
0.94 Tfap2A alone has the ability to promote generation of GABAergic interneurons while Tfap2B, but not Tfap2A, can suppress the generation of excitatory cells.
0.93 Tfap2A+ and Tfap2B+ cells in the early developing cerebellum, we differentiated regions of the embryonic cerebellum with relevant molecular markers of GABAergic lineage at E12.5.
0.93 Tfap2B, but not Tfap2A can suppress the expression of Pax6.
0.92 Tfap2A and Tfap2B in the Specification of GABAergic Interneurons in the Developing Cerebellum
0.92 Tfap2A and Tfap2B in GABAergic Precursors
0.92 Tfap2A and Tfap2B Expression on Specification of GABAergic Interneurons
0.91 Tfap2A and Tfap2B during the development of cerebellar GABAergic neuronal subtypes.
0.91 Tfap2A and Tfap2B are expressed in the rhombic lip (RL) and the intermediate domain of rhombomere (r)1, where the first cerebellar neurons such as glutamatergic DCN neurons and GABAergic Purkinje cells are generated at embryonic day (E) 10.5 (Hoshino et al.,; Machold and Fishell,; Wang et al.,).
0.91 Tfap2A and Tfap2B in Establishment of GABAergic Neuronal Subtype Identity
0.90 Tfap2A and Tfap2B is maintained during late embryogenesis through postnatal stages, we analyzed their expression in perinatal and postnatal cerebellar tissues.
0.90 Tfap2A+ and Tfap2B+ cells at E12.5 are GABAergic, and Tfap2A labels postmitotic cells while Tfap2B labels both mitotic and postmitotic cells in the VZ.
0.90 Tfap2A or Tfap2B is sufficient to regulate Pax2 expression.
0.89 Tfap2A and Tfap2B during the development of GABAergic neuronal subtypes, we set out to manipulate the expression of Tfap2A and Tfap2B via IUE.
0.87 Tfap2A+ and Tfap2B+ cells also overlap with Pax2 indicating that these cells identify for interneuron precursors (Supplementary Figure S3).
0.87 Tfap2A and Tfap2B misexpression on generation of cerebellar neuronal subpopulations.
0.87 Tfap2 for specification of GABAergic neurons, we assessed the effects of knocking down the expression of Tfap2A or Tfap2B on the expression of Pax2, Pax6 and CBP at E15.5.
0.85 Tfap2A and Tfap2B in the Developing and Mature Cerebellum
0.85 Tfap2A is indispensable for craniofacial, eye, and limb development (Schorle et al.,; Nottoli et al.,); and, Tfap2B is indispensable for kidney development (Moser et al.,).
0.84 Tfap2A expression (K) is detected in the ML, PCL and IGL whereas Tfap2B expression (L) is restricted to the ML and IGL.
0.84 Tfap2A+ and Tfap2B+ Neurons in the Developing Cerebellum
0.82 Tfap2A and Tfap2B in the mouse cerebellum.
0.82 Tfap2A and Tfap2B with cell-type specific molecular markers in the adult cerebellum.
0.81 Tfap2A and Tfap2B are unable to influence CBP expression.
0.80 Tfap2A misexpression results in an increase in Pax2 expression, while Tfap2B misexpression results in a decrease in the expression of Pax6.
0.78 Tfap2A and Tfap2B with cell type-specific molecular markers in the adult cerebellar cortex.
0.77 Tfap2A and Tfap2B in the development of cerebellar neurons.
0.75 Tfap2A nor Tfap2B is observed in NeuN+ granule cells (Figures 2G-I,P-R).
0.73 Tfap2A, but not Tfap2B, labels small GABAergic neurons in all three nuclei (Supplementary Figure S2).
0.66 Tfap2A and Tfap2B, respectively (Figures 5K-M,Q-S).
0.65 Tfap2A (green, A) and Tfap2B (magenta, B) is not detected in the cerebellar derivatives in r1 at E10.5.
22411557 0.98 AP-2alpha or AP-2beta-positive cells did not express Ki67, suggesting that both family members are a feature of postmitotic retinal cells.
0.98 AP-2alpha, AP-2beta expression was detected in both glycinergic and GABAergic amacrine cells in the adult retina (Fig. 1F,G).
0.98 AP-2alpha and AP-2beta, AP-2gamma expression was detected in both the GABAergic (GAT-1-positive) and glycinergic (GLYT1-positive) amacrine cell subsets in the mature mouse retina (Fig. 4B,C).
0.98 AP-2 family members (AP-2alpha, AP-2beta, AP-2gamma, and AP-2delta) are expressed in the developing retina, and that three of these (AP-2alpha, AP-2beta, and AP-2gamma) are present in INL cell types while AP-2delta is confined to RGCs.
0.98 AP-2alpha and AP-2beta, this family member is expressed in postmitotic amacrine cells of the GABAergic and glycinergic classes (Figs. 3, 4).
0.98 AP-2alpha, AP-2beta is expressed in postmitotic transition cells during retinogenesis (Fig. 1).
0.98 AP-2alpha and AP-2beta are expressed in newly generated amacrine transition cells as they approach the presumptive INL, and both proteins are maintained in amacrine cells throughout postnatal development and into adulthood.
0.98 AP-2alpha and AP-2beta have also been implicated in the development of noradrenergic neurons within the mouse and zebrafish hindbrain, and AP-2delta is required for cell survival in the posterior midbrain.
0.98 AP-2 family members was recently reported in the developing peripheral nervous system, where AP-2alpha and AP-2beta have partially redundant roles in the survival of neural crest-derived sympathetic neurons.
0.97 AP-2alpha and AP-2beta are also co-expressed in developing horizontal cells.
0.97 AP-2 activity in retinogenesis, delineating the overlapping expression patterns of Tcfap2a, Tcfap2b, and Tcfap2c in the neural retina, and revealing a redundant requirement for Tcfap2a and Tcfap2b in horizontal and amacrine cell development.
0.97 AP-2alpha is expressed in postmitotic developing amacrine cells, and that AP-2alpha and AP-2beta are expressed in overlapping populations of cells in the neonatal and adult retina.
0.97 AP-2beta were also more weakly immunoreactive to anti-AP-2alpha (Fig. 2D, arrowheads and inset), suggesting that AP-2alpha is co-expressed with AP-2beta in developing horizontal cells.
0.97 AP-2alpha and AP-2beta exhibit highly overlapping expression patterns in postmitotic amacrine and horizontal cells.
0.97 Tcfap2a and Tcfap2b from the developing retina caused a striking loss of horizontal cells and defective amacrine cell development.
0.97 AP-2alpha and AP-2beta are well correlated with amacrine and horizontal cell differentiation.
0.97 Tcfap2a and Tcfap2b are expressed in glycinergic and GABAergic amacrine cells and are also co-expressed with markers of many other smaller amacrine subpopulations including cholinergic (ISL1-positive, SOX2-positive), NR4A2-positive, CALB2-positive, and AII (DAB1-positive) amacrines.
0.97 Tcfap2a, or neural crest progenitors with Tcfap2b, induces neuronal differentiation.
0.96 AP-2alpha and AP-2beta proteins are expressed in developing and mature mouse retinal amacrine cells of the INL and GCL, and we also detected transcripts of Tcfap2c (AP-2gamma) and Tcfap2d (AP-2delta) in the embryonic and adult murine retina.
0.96 AP-2alpha and AP-2beta are also co-expressed in developing horizontal cells.
0.96 AP-2alpha and AP-2beta expression in the developing retina, a large proportion of the Tcfap2a-null cells expressing beta-galactosidase would also normally co-express functional AP-2beta protein and are, therefore, double "Tcfap2a/b null" cells.
0.96 AP-2alpha and AP-2beta activity for horizontal cell development.
0.96 AP-2alpha and AP-2beta are redundantly required for amacrine cell development.
0.96 AP-2alpha and AP-2beta compared with those singly labeled for AP-2alpha or AP-2beta (Fig. 2), thereby demonstrating their extensive overlap and supporting compensation by one protein when the other is deficient in the retina.
0.96 AP-2alpha and AP-2beta.
0.96 Tcfap2a and Tcfap2b are redundantly required for the determination or maintenance of the entire horizontal cell population.
0.96 Tcfap2a, Tcfap2b, and Tcfap2c in retinogenesis, delineating their overlapping and unique expression patterns in developing horizontal and amacrine cell populations, and revealing a redundant requirement for Tcfap2a and Tcfap2b in horizontal and amacrine cell development.
0.95 Tcfap2a did not affect retinogenesis, two other family members, AP-2beta and AP-2gamma, showed expression patterns similar to AP-2alpha.
0.95 AP-2alpha and AP-2beta expression.
0.95 AP-2alpha expression diminished shortly after birth and only AP-2beta protein was retained in mature horizontal cells, a finding that concurs with data from the chick retina.
0.94 AP-2alpha and AP-2beta were detected in SOX2-positive cholinergic amacrines (Fig. 4K-M, arrowheads).
0.94 AP-2alpha and AP-2beta are expressed in developing mouse horizontal cells, although AP-2alpha expression is transient
0.94 Tcfap2a and Tcfap2b leads to loss of retinal horizontal cells.
0.93 Tcfap2a or Tcfap2b appears to rescue horizontal cells to some extent.
0.92 AP-2alpha and AP-2beta Are Expressed in Postmitotic Amacrine and Horizontal Cells
0.92 Tcfap2a and Tcfap2b impacted the development of cell types other than amacrine and horizontal cells, we analyzed the expression of additional retinal markers.
0.91 AP-2alpha-positive and AP-2beta-positive cells colocalizing with Ki67, which is expressed by cells in all phases of the cell cycle (; Supp.
0.91 AP-2alpha expression in mouse horizontal cells, we first performed double immunostains for AP-2alpha and AP-2beta at birth, when strongly immunoreactive AP-2beta-positive cells are present in the future horizontal cell layer.
0.91 AP-2alpha and AP-2beta, AP-2gamma expression is not a feature of mitotic RPCs.
0.90 Tcfap2a and Tcfap2b.
0.89 AP-2alpha and AP-2beta in horizontal cells of the mouse retina (Figs. 1, 2).
0.89 AP-2beta (Fig. 5) also emphasized the fact that the AP-2gamma-positive amacrine cell population is partially distinct from the extensively colocalized AP-2alpha/beta-positive population, particularly in the adult retina where less than 4% of the AP-2gamma and/or AP-2beta-positive population overlaps (Fig. 5).
0.88 AP-2alpha and AP-2beta, where we detected extensive colocalization by embryonic day (E) 15.5 (Fig. 1A).
0.88 AP-2alpha and AP-2beta clearly have the most similar retinal expression patterns among the AP-2 family members, we sought to determine the effects of combined Tcfap2a and Tcfap2b deletion in the developing retina.
0.86 Tcfap2a, Tcfap2b and Tcfap2c transcripts, we examined AP-2gamma protein expression in the developing and mature mouse retina.
0.78 Tcfap2a, Tcfap2b, and Tcfap2c in the developing NR, through detailed expression analyses and generation of a double Tcfap2a/b mutant mouse model that was studied until its death at postnatal day 0 (P0).
0.77 AP-2alpha- and AP-2beta-immunoreactive cells than previously appreciated in the neonatal retina (Fig. 2D), possibly due to the stage examined and the fact that we find our anti-AP-2 antibodies to work particularly well on P0 enucleated eyes.
0.77 AP-2alpha and AP-2beta were expressed in this subtype (Fig. 4).
0.76 Tcfap2a and Tcfap2b Causes Amacrine Cell Defects
0.75 AP-2alpha and AP-2beta, AP-2gamma expression was not detected in the retina at E12.5 (not shown); however by E15.5, AP-2gamma-immunoreactive cells were scattered in the inner and outer neuroblast layers (Fig. 3A).
0.75 AP-2alpha and AP-2beta in developing amacrine cells, we examined Tcfap2a/b mutant retinas for amacrine cell abnormalities.
0.68 AP-2alpha, AP-2beta, and AP-2gamma in amacrine cell subpopulations at birth.
0.66 AP-2alpha and AP-2beta, AP-2gamma expression initiated later and was not a marker of developing horizontal cells (Fig. 3).
0.63 Tcfap2a and Tcfap2b, whereas Tcfap2d, the most divergent AP-2 family member, was largely confined to the GCL.
0.63 AP-2alpha and AP-2beta redundancy into the postnatal period to analyze the morphology, positioning, and population sizes of a spectrum of amacrine cell subtypes, and also to assess visual function.
0.55 Tcfap2a conditional KO mice were crossed onto a Tcfap2b germ-line KO background to obtain Tcfap2aki7lacZ/lox/Tcfap2b-/-/alpha-Cre+/- mice, referred to herein as Tcfap2a/b mutants (Supp.
0.53 AP-2alpha-positive and AP-2beta-positive populations in the developing and adult retina, which showed that over 80% of AP-2alpha and/or AP-2beta-positive cells were co-labeled during development, while adult retinas exhibited 77 +- 1% overlap (Fig. 2G).
29715367 0.98 AP-2) transcription factors, AP-2alpha and AP-2beta, is important in early retinal development, specifically in the formation of horizontal cells.
0.98 AP-2alpha and AP-2beta are coexpressed in the embryonic and adult retina, initially in the inner nuclear layer (INL) and a subset of cells in the ganglion cell layer (GCL), both of which correspond to expression in ACs and HCs.
0.98 AP-2alpha and AP-2beta transcription factors results in a significant disruption in the mosaic spacing of cholinergic ACs, specifically within the INL layer.
0.98 AP-2 transcription factors, in particular AP-2alpha and AP-2beta, exhibit overlapping expression in the AC and HC populations of the embryonic murine retina, continuing into the postnatal stages.
0.97 AP-2alpha and AP-2beta from the retina resulted in a variety of abnormalities, including the absence of horizontal cells, defects in the photoreceptor ribbons in which synapses failed to form, along with evidence of aberrant amacrine cell arrangement.
0.97 AP-2alpha and AP-2beta in both the glycinergic and GABAergic AC populations, with a 77% overlap in their expression profiles.
0.97 AP-2alpha and AP-2beta from the retina of embryonic mice results in an absence of HCs and abnormal cellular arrangement of cholinergic ACs as was observed in histological sections immunolabeled with SOX2 and ISL1/2.
0.97 AP-2alpha and AP-2beta (DBL alpha/beta KO) in the retina exhibited loss of HCs, aberrant AC mosaics, and altered sublamination, which culminated in abnormal retinal function, as determined by ERG.
0.97 AP-2alpha and AP-2beta in ACs.
0.97 AP-2alpha and AP-2beta.
0.97 AP-2alpha and AP-2beta have been shown in both embryonic and adult mice to have similar expression patterns in the AC population.
0.96 AP-2alpha and AP-2beta in proper amacrine mosaic patterning and a normal functional light response in the retina.
0.96 AP-2alpha and AP-2beta in the developing retina resulted in an absence of HCs in embryonic sections.
0.96 AP-2alpha and AP-2beta resulted in an absence of calbindin staining in the retinal region in which HCs are typically present (Figs. 4C, 4D).
0.96 AP-2alpha and AP-2beta From the Retina
0.96 AP-2alpha and AP-2beta, resulting in a decrease in b-wave amplitudes.
0.96 AP-2alpha and AP-2beta of interneuron patterning during retinal development.
0.95 AP-2alpha and AP-2beta in the Developing Murine Retina Leads to Altered Amacrine Cell Mosaics and Disrupted Visual Function
0.95 AP-2alpha and AP-2beta, the b-wave amplitude, representative of interneuron signal processing, was significantly reduced compared with control littermates.
0.95 AP-2 family consists of a class of five different transcription factors: AP-2alpha, AP-2beta, AP-2gamma, AP-2delta, and AP-2epsilon, which form homo- or heterodimers.
0.95 AP-2alpha and AP-2beta revealed that although AC population numbers were not significantly affected, their distribution in the INL and GCL was disorganized when compared with controls.
0.94 AP-2alpha and AP-2beta from the retina may decrease the physiologic response to light, and that AP-2beta may be more significant in this process than AP-2alpha.
0.94 AP-2alpha and AP-2beta, in the adult retina HCs exclusively express AP-2beta.
0.94 AP-2alpha and AP-2beta did not affect the birth of ACs during retinogenesis, it did affect the regulation of AC mosaic formation.
0.93 AP-2alpha and AP-2beta expression was readily detected in the INL and GCL of control retinas; however, a clear deletion of both was observed in DBL alpha/beta KO retinas.
0.93 AP-2alpha (green) and AP-2beta (red) exhibit overlapping expression patterns in the adult mouse retina (arrow).
0.93 AP-2alpha and AP-2beta mice exhibited a significant difference in AC mosaics as revealed by both NN distances and VD areas analyses, methods to measure retinal mosaics, and spacing of homotypic cells.
0.92 AP-2alpha, AP-2beta, or AP-2alpha/beta from the retina.
0.91 AP-2beta, we have generated a new model for conditional deletion of AP-2alpha and AP-2beta from the retina, in which mice survive postnatally (DBL alpha/beta mice).
0.90 AP-2alpha and AP-2beta From the Retina
0.86 AP-2alpha and AP-2beta in the retina, a complete absence of HC was observed and potential defects in AC positioning and homotypic spacing were suspected.
0.84 AP-2alpha and AP-2beta Expression
0.83 AP-2alpha/AP-2beta from the retina.
0.82 AP-2alpha and AP-2beta exhibit overlapping expression patterns in the AC and HC populations, we surmised that AP-2beta might play a potential compensatory role.
0.81 AP-2alpha/AP-2beta expression ablated all AC populations.
0.81 AP-2alpha or AP-2beta alone was not sufficient to create changes in the mosaic patterning of cholinergic ACs.
0.78 AP-2alpha and AP-2beta From the Retina
0.74 AP-2alpha and AP-2beta in both AC mosaics, as well as for HC cell genesis in the retina.
0.71 AP-2alpha/AP-2beta in the retina.
0.70 AP-2alpha expression in the INL and GCL, whereas AP-2beta expression remained comparable to that of controls.
0.69 AP-2alpha and AP-2beta from the retina to further examine the combinatory role of these genes in retinal cell patterning and function in postnatal adult mice as measured by Voronoi domain area and nearest-neighbor distance spatial analyses and ERGs, respectively.
0.68 AP-2alpha and AP-2beta affects retinogenesis postnatally.
0.65 AP-2alpha and AP-2beta influence AC mosaic formation.
0.53 Tfap2a and Tfap2b small hairpin RNAs (shRNAs) into the retina to knock down expression of AP-2alpha and AP-2beta.
29467543 0.98 AP-2 family (AP-2alpha, AP-2beta, AP-2gamma and AP-2delta) have previously been shown to be expressed in developing retina.
0.98 AP-2alpha and AP-2beta, especially at early stages of retinal development.
0.98 AP-2alpha, AP-2beta and AP-2gamma are expressed in neural crest cell lineages, the peripheral nervous system, facial and limb mesenchyme, the epithelia of the developing embryo and/or extraembryonic trophectoderm.
0.98 AP-2 family has previously been documented in the developing retina, with AP-2alpha, AP-2beta and AP-2gamma all expressed in amacrine cells.
0.98 AP-2alpha and AP-2beta.
0.98 AP-2alpha, AP-2beta and AP-2gamma, AP-2epsilon is specifically expressed in a subset of amacrine cells.
0.98 AP-2alpha or AP-2beta expression constructs in retinoblastoma cells induced apoptosis, suggesting incompatibility with expression of AP-2 amacrine cell differentiation markers and survival in retinoblastoma cells.
0.97 AP-2alpha, AP-2beta and AP-2delta in retinal cell specification and function.
0.97 AP-2alpha, AP-2beta and AP-2gamma-positive cells, suggesting a specialized role for AP-2epsilon in a subset of amacrine cells.
0.96 AP-2alpha, AP-2beta and AP-2gamma.
0.96 AP-2alpha and AP-2beta are widely distributed in amacrine cells, with AP-2alpha/AP-2beta co-expression observed in a high percentage of cells.
0.96 AP-2alpha, AP-2beta and AP-2gamma can all bind as either homodimers or heterodimers to an AP-2 recognition site in the c-erbB2 promoter; however, AP-2alpha and AP-2gamma are four times more active than AP-2beta at activating a c-erbB2-driven reporter construct.
0.96 AP-2alpha, AP-2beta and AP-2gamma are found in both GABAergic and glycinergic amacrine cells.
0.96 AP-2s previously shown to be expressed in amacrine cells, with extensive overlap with AP-2alpha and AP-2beta at all stages tested.
0.95 AP-2alpha and AP-2beta in amacrine and horizontal cell differentiation.
0.95 AP-2alpha (72.9%), AP-2beta (82.5%) and AP-2gamma (41.7%) at P14 suggest that a significant proportion of AP-2epsilon-positive amacrine cells co-express three or more AP-2's.
0.95 AP-2alpha, AP-2beta and AP-2gamma, respectively, suggesting the possibility of significant overlap in AP-2alpha and AP-2epsilon expression for this particular subset of amacrine cells.
0.95 AP-2 expression in mouse retina, there were clusters (e.g. cluster 6) with elevated levels of AP-2alpha, AP-2beta and AP-2gamma sequences.
0.95 AP-2alpha and AP-2beta (AP-2beta/AP-2gamma co-localization is described in Bassett et al.; AP-2alpha/AP-2gamma co-localization is shown in Fig. 8).
0.95 AP-2alpha and AP-2beta, other members of the AP-2 family may compensate for loss of AP-2epsilon expression.
0.93 AP-2alpha and AP-2beta knockout mice show horizontal and amacrine cell defects that were not observed upon deletion of AP-2alpha alone.
0.93 AP-2alpha and AP-2beta-positive cells can be either glycinergic or GABAergic.
0.92 AP-2alpha and AP-2beta, whereas AP2delta is found in a subset of ganglion cells.
0.90 AP-2alpha, beta, gamma in the developing retina, with strongest associations observed with AP-2alpha and AP-2beta at P7 and P14.
0.86 AP-2alpha and AP-2beta, with little co-expression observed at early developmental stages.
0.80 AP-2alpha or AP-2beta (clusters 17 and 18).
0.75 AP-2alpha and AP-2beta are restricted to amacrine cells and horizontal cells.
28249010 0.98 TFAP2A and TFAP2B act redundantly subsequent to neural crest induction within distinct neural crest lineages.
0.98 Tfap2a/Tfap2b DCM embryos implies that they contribute to specification and differentiation of the melanocyte lineage, similar to the functions of MITF.
0.97 Tfap2a and Tfap2b are expressed in early neural crest as well as the melanocyte lineage, resulting in almost complete loss of migrating trunk neural crest prior to specification of the melanocyte lineage in Tfap2a/Tfap2b double mutants.
0.97 TFAP2A and TFAP2B redundantly regulate murine melanocyte development.
0.96 Tfap2a and Tfap2b are both expressed in mouse melanocytes, and we show that mouse embryos with Wnt1-Cre-mediated deletion of Tfap2a and Tfap2b in the neural crest almost completely lack melanocytes but retain neural crest-derived sensory ganglia.
0.94 Tfap2a or Tfap2b alone does not greatly impact embryonic development of the melanocyte lineages, but the combined knockout of both genes causes a significant loss of melanocytes.
0.93 Tfap2a/Tfap2b DCM mice could reflect a requirement for TFAP2 in neural crest survival or lineage specification of certain derivatives.
0.86 Tfap2a and Tfap2b have the highest and second highest expression, respectively, while Tfap2c and Tfap2e are undetectable.
0.85 Tfap2a / Tfap2b double conditional mutants are depleted of melanocytes
0.79 Tfap2a/Tfap2b DCM embryos have many fewer beta-gal-positive cells in this location (Fig 4D).
22325097 0.98 AP-2 and we observed that cAMP increased AP-2beta levels in the nuclear fraction of astrocytes (data not shown).
0.98 AP-2beta in the nucleus is seen by our results showing that cells expressing AP-2 and incubated with Abeta(42) had enhanced activation of the apoE promoter region containing AP-2 binding sites in comparison with AP-2 deficient cells.
0.96 AP-2alpha levels and significantly increased AP-2beta levels in the nuclear fraction.
0.96 AP-2alpha levels (Fig. 2A) and significantly increased AP-2beta levels (Fig. 2B) in the nuclear extract.
0.93 AP-2 isoforms, AP-2alpha and AP-2beta are the most abundant isoforms in the brain; AP-2gamma is co-expressed with AP-2alpha and AP-2beta in several brain regions, but its expression level is the lowest among the three.
0.93 AP-2alpha and AP-2beta in the cell lysates of Abeta treated and control cells did not differ (Fig. 2C and 2D) suggesting that the Abeta-induced increase of AP-2beta and the reduction of AP-2alpha in the nuclear fraction were due to a redistribution of the proteins and not synthesis or inhibition of degradation.
0.91 AP-2beta levels but significantly reduced AP-2alpha levels in the nuclear extract.
0.86 AP-2alpha/AP-2beta and the mechanism that induces movement of AP-2alpha out of the nucleus.
0.54 AP-2alpha showed a modest but significant decrease in the nucleus while AP-2beta showed a significant increase.
20875861 0.98 AP-2beta, a member of the AP2 family, plays a critical role in the development of sympathetic neurons and locus coeruleus and their norepinephrine (NE) neurotransmitter phenotype.
0.98 AP2 family (AP-2alpha, beta, and gamma) that are expressed in the nervous system, AP-2beta specifically regulates development of sympathetic neurons that are derived from SA progenitors.
0.97 AP-2 binding site in the 2kb upstream promoter of the rat DBH gene, which is present in the human DBH promoter, suggests that the promoter structure and regulation mechanisms of human and rat DBH genes by AP-2beta may be significantly different.
0.96 AP-2beta to the AP2 binding sites of the rat PNMT promoter.
0.87 AP-2alpha was first isolated, four other homologous genes, AP-2beta, AP-2gamma, AP-2delta, and AP-2epsilon, have been reported as members of the AP2 family.
0.84 AP-2alpha in chromaffin cell development because expression of AP-2alpha is detected in adrenal medulla by immunohistochemical method and by RT-PCR, although its signal is significantly weaker than AP-2beta (data not shown).
0.66 AP-2alpha and AP-2beta show similar transactivation and DNA binding activities in vitro (data not shown).
27483349 0.98 AP-2 family, particularly AP-2alpha and AP-2beta, can regulate several aspects of eye development through their function in the surface ectoderm or neural retina.
0.98 AP-2beta can act in the retina in conjunction with AP-2alpha to regulate the development of specific neuronal cell types.
0.97 AP-2 transcription factor family, consisting of five genes encoding the proteins AP-2alpha, AP-2beta, AP-2gamma, AP-2delta and AP-2epsilon, respectively, is postulated to be a crucial component of the gene regulatory network responsible for the evolution and function of the neural crest in vertebrates.
0.97 AP-2alpha and AP-2beta function together in vivo to control development of horizontal and amacrine cell populations in the embryonic retina and potentially in the post-natal eye.
16420676 0.98 AP-2 family members (AP-2alpha, AP-2beta and AP-2gamma) are coexpressed in neural-crest cells, the peripheral nervous system, facial and limb mesenchyme, various epithelia of the developing embryo and the extraembryonic trophectoderm.
0.97 AP-2alpha, AP-2beta, AP-2gamma, AP-2delta and AP-2epsilon.
0.90 AP-2alpha, AP-2beta, AP-2gamma, AP-2delta and AP-2epsilon; frogs and fish have some of these proteins, and homologs are also known in invertebrates.
21829553 0.98 Tfap2b or Tfap2a expression plasmids with the promoter constructs into NIH3T3 (ATCC) or HepG4 (ATCC) cells demonstrated that Bmp2 promoter activities were increased 3 to 6 fold in a dose dependant manner (P<0.01).
0.98 Tfap2a and Tfap2b are expressed in cardiac neural crest cells in the pharyngeal arches surrounding the pharyngeal arch arteries, which later populate the aortopulmonary septum and conotruncal cushions prior to and during overt septation of the outflow tract.
0.95 Tfap2a and Tfap2b knockout mice show different cardiac phenotypes, it is most likely that the two genes play different roles within cardiac neural crest cells.
21858141 0.98 Ap-2alpha, Ap-2beta, Ap-2gamma and Ap-2delta are expressed in the anterior midbrain (colliculus superior) of E17 embryos.
0.97 Ap-2alpha, Ap-2beta and Ap-2gamma show partially overlapping expression patterns in neural crest cells, the central and peripheral nervous system, the facial mesenchyme, the limbs, various epithelia of the developing embryo, and the extraembryonic trophectoderm.
0.96 Ap-2alpha, Ap-2beta, Ap-2gamma and Ap-2delta expression in the anterior dorsal midbrain but not in the posterior midbrain, the colliculus inferior (Fig. 3b).
26968737 0.98 Tfap2b as an attractive candidate for further analysis because it encodes AP-2beta, a member of the AP-2 family of transcription factors that are widely required for normal eye development, and it is expressed at the appropriate time in neural crest mesenchyme of the developing cornea.
0.98 AP-2alpha and AP-2beta in certain tissues, with the net effect dependent on context.
0.96 AP-2alpha permits angiogenesis and metastasis in cancers such as nasopharyngeal carcincoma and melanoma, whereas the overexpression of AP-2beta promotes angiogenesis in lung adenocarcinomas.
27259519 0.98 AP-2alpha, AP-2beta and AP-2gamma are the most widely expressed and best-characterized of the five AP-2 transcription factors, with all three AP-2s implicated in neural crest formation.
0.98 AP-2 family virtually absent in the inferior colliculus, AP-2beta, was expressed throughout most of the SC (Additional file 1: Figure S6).
0.97 AP-2alpha, AP-2beta, AP-2gamma and AP-2epsilon in mice indicates roles in craniofacial and limb development, renal and adrenal chromaffin cell differentiation, formation of extraembryonic lineages and primordial germ cell specification, and organization of the olfactory bulb, respectively.
28649789 0.98 TFAP2A, TFAP2B, TFAP2C, and TFAP2E are all expressed in NC and contribute to multiple steps in the NC lineage leading to melanocytes, including melanocyte differentiation.
0.97 Tfap2a and Tfap2b resulted in increased apoptosis of migratory NC, leading to almost complete loss of sympathetic and sensory ganglia.
30127719 0.98 Tfap2a, Tfap2b, Tfap2c, Nr4a2, Neurod2, Prox1, Sall3, Onecut2 (Figures 6D,E), which are involved in the specification and differentiation of amacrine and/or horizontal cells, suggesting that there may be supernumerary amacrine and horizontal cells generated from progenitors in Ldb1Deltafl/Deltafl retinas at P0 despite their loss at P21.
0.97 Tfap2a, Tfap2b, Neurod2, Prox1, Sall3, and Onecut2 in the null retina (Figure 6G).
31924792 0.98 Tfap2a, and Tfap2b, previously shown to be negative regulators of myelination or transcription factors known for their function in early NC development.
0.98 Tfap2a, Tfap2b, Myc, and Cebps transcription regulators known to play key roles in SCs or early NC development was noticed.
20678241 0.98 AP-2alpha, AP-2beta and AP-2gamma) are co-expressed in neural crest cells, the peripheral nervous system, as well as facial and limb mesenchyme, where they play crucial roles during development.
21682828 0.98 AP-2alpha is co-expressed with AP-2beta and AP-2gamma in neural-crest cells, the peripheral nervous system, facial and limb mesenchyme, various epithelia of the developing embryo and the extra-embryonic trophectoderm.
25966682 0.98 Tfap2a and Tfap2b transcription factors as two major downstream effectors of Ptf1a.
27941807 0.98 TFAP2A, and TFAP2B (Fig. 4d); HAND1, POSTN, and TFAP2A are markers for early mouse amnion, and POSTN, TFAP2A, and TFAP2B are reported first trimester human amnion markers.
28387218 0.98 AP-2 mediates retrograde transport of TrkB-containing autophagosomes via association of AP-2alpha with LC3 and of AP-2beta with the p150Glued subunit of the dynein cofactor dynactin to promote neuronal complexity and counteract neurodegeneration in vivo.
29518009 0.98 AP-2alpha, AP-2beta, AP-2gamma, AP-2delta, and AP-2epsilon; which play important roles in several cellular processes, such as apoptosis, migration, and differentiation.
30283876 0.98 AP2alpha, AP2beta, and AP2 mu subunits that is pivotal for clathrin-mediated endocytosis.
30306639 0.98 Tfap2a, Tfap2b) that are expressed in early SC development were also induced at a low level.
23533700 0.97 AP-2) family of transcription factors, consisting of five different members AP-2alpha, AP-2beta, AP-2gamma, AP-2delta, and AP-2epsilon, stimulate proliferation and suppress terminal differentiation in a cell-type-specific manner during embryonic development.
0.97 AP-2alpha is confined to basal epithelial cells while AP-2beta is broadly expressed throughout all cell layers.
20525283 0.97 Tcfap2a or Tcfap2b or Tcfap2 g mice.
21654541 0.97 AP-2 family members display specific expression patterns: AP-2alpha, AP-2beta, AP-2gamma are expressed essentially in neural-crest cells, peripheral nervous system, facial and limb mesenchyme, AP-2delta in the heart, central nervous system, and retina, and AP-2epsilon in the olfactory bulb.
29660784 0.97 TFAP2A and TFAP2B.
30786278 0.97 Tfap2A, Tfap2B, Erg, and Cdh6) are upregulated in the cornea, whereas the remaining 13 (28%) genes, including Axud1, Foxd3, Gbx2, and Rxrg, are not expressed (Supplementary Table S2).
16449191 0.96 AP-2 family members in skin also remains unknown, as AP-2beta-null mice do not display a skin phenotype, and targeting of AP-2gamma results in lethality before epidermal and follicle development.
0.89 AP-2beta results in massive apoptosis in the kidney and why the loss of AP-2alpha in neural crest impaired craniofacial development and pigmentation.
20175189 0.96 AP-2 gene family, particularly AP-2beta and AP-2gamma, are expressed in a similar spatiotemporal pattern to that of AP-2alpha, it is possible that there is functional redundancy between these family members with respect to mouse Inka1 expression.
0.83 Tcfap2a and Tcfap2b indicates that Inka1 expression is still maintained in these mutants, too (B. R., unpublished).
20459791 0.96 Activator Proteins-2 (AP-2, Tcfap2) comprises 5 highly conserved DNA-binding transcription factors referred to as AP-2alpha, AP-2beta, AP-2gamma, AP-2delta and AP-2epsilon (or Tcfap2a-e).
28894266 0.96 AP-2) which consists of 5 members (AP-2alpha, AP-2beta, AP-2gamma, AP-2delta and AP-2epsilon).
29059322 0.96 Ap-2 (tfap2b) (Figure 1D).
30443989 0.96 AP2a knockout mice developed severe skeletal defects with bone-associated symptoms of craniofacial dismorphogenesis and duplicated limbs, forepaws or fingers.16, 17 The mutations of AP2a in human develop into the Branchio-Oculo-Facial Syndrome (BOFS) showing orofacial clefting similar with AP2a-null mice.18, 19, 20 AP2a was also found to suppress chondrogenesis by downregulating the associated key transcription factor Sox5 and Sox6, as well as the matrix protein Col-II and Col-X.21 A most recent investigation found that the cooperation of AP2a and AP2b is the major regulator in neural crest development and affects the jaw skeleton patterning through the DLX code.22 All the studies showed the importance of AP2a in hard tissue differentiation and development.
19580868 0.95 AP-2 genes, Tcfap2a, Tcfap2b, and Tcfap2c - encoding AP-2alpha, AP-2beta and AP-2gamma, respectively - are essential for embryogenesis and post-natal viability.
20571064 0.95 AP-2 alpha nor AP-2 beta expression constructs affected WT1-mediated transactivation (data not shown), indicating that these proteins are unlikely to be functional cofactors in Scribble gene regulation.
29048434 0.94 TFAP2B, TFAP2A, RUNX1 and RUNX3).
32085610 0.93 Tfap2b (transcription factor AP-2 beta), (Table 7).
0.93 Tfap2b (transcription factor AP-2 beta) were significantly down-regulated.
21489314 0.93 TFAP2alpha, TFAP2beta, TFAP2gamma, TFAP2delta and TFAP2epsilon.
27176626 0.92 AP-2alpha and AP-2beta expression in mouse embryos overlap significantly,, but the single knockout models of each gene did not share any phenotypic defects, suggesting non-redundant roles of the two genes.
0.89 AP-2alpha, AP-2beta, AP-2gamma AP-2delta and AP-2epsilon.
25187989 0.88 AP-2beta would bind to be either sumoylated, in a fashion similar to the Kctd1 and AP-2alpha, or possibly ubiquitinated.
28818080 0.88 Tfap2a, Tfap2b or Tfap2c exhibit lethal phenotypic defects in neural tube, face, eye, heart, skin, urogenital tissues or extraembryonic trophoblasts and usually die at birth.
18270576 0.87 TCFAP-2beta or Nrl were predicted based upon previous work that characterized them as having either AC expression (Lrrn3, TCFAP-2alpha and Bruno-like 4 for example) or rod photoreceptor cell expression (Crx, IRBP, Pde6a, Rom1, and Tulp1 for example).
27852742 0.81 AP-2beta and NF-kappaB, showed similar wtDC/TNFko DC-extract binding profiles, but their binding of wtDC-extract was notably lower than that of the AP-2alpha DNA probe.
28412966 0.75 TFAP2A, TFAP2B, TFAP2C, TFAP2D and TFAP2E, or AP-2alpha, AP-2beta, AP-2gamma, AP-2delta and AP-2epsilon, respectively.
28363736 0.54 Tfap2a, Tfap2b, Tfap2c, Tp63, Ovol1, Ripk4, Jag2) belong to our pan-ectodermal gene class.



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