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Members of the ZAS family, such as ZAS2 (HIVEP2), are large proteins that contain a ZAS domain, a modular protein structure consisting of a pair of C2H2 zinc fingers with an acidic-rich region and a serine/threonine-rich sequence. Additionally we are shipping Human Immunodeficiency Virus Type I Enhancer Binding Protein 2 Antibodies (12) and many more products for this protein.
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the Shn2 deficiency attenuates bidirectional short-term synaptic plasticity at the medial perforant path-granule cell synapse.
Shn2 knockout mice serve as a unique tool for investigating morphological abnormalities of subcellular-scale structures in schizophrenia, intellectual disability, and its related disorders.
Schnurri-2 knockout mice have behavioral abnormalities that resemble those of schizophrenics.
Shn-2 plays an important role in the activation and function of NK cells and the development of T cell lymphoma in vivo.
repression of T cell receptor-induced death pathways is critical for proper interpretation of positive selecting signals in vivo; identification of schnurri-2 (Shn2; or Hivep2) as a crucial death dampener
Shn2-deficient mice maintain bone mass at the levels comparable to wild-type sham mice even after ovariectomy-induced bone loss.
Results indicate that Schnurri-2-mediated repression of NF-kappaB is required for cell survival and the successful generation of memory Th1/Th2 cells.
report that mice bearing parallel null mutations in the adapter proteins Schnurri2 (Shn2) and Schnurri3 (Shn3) exhibit defects in patterning of the axial skeleton during embryogenesis.
Data suggest that Schnurri-2 plays a crucial role in the control of T helper type 2 cell differentiation by regulating NF-kappaB function.
Shn-2 plays a critical role in locomotion and anxiety-like behavior. Stress-induced corticosterone levels were significantly higher in Shn-2(-/-) mice compared to wild-type controls.
Shn-2 appears to control the generation of memory Th1/Th2 cells through a change in their susceptibility to cell death.
Shn-2 in Th2 cells plays an important role as a negative regulator in allergic airway inflammation.
These results newly identify Schnurri-2 and CLIC4 as modifiers of TGF-beta signalling through their stabilization of p-Smad2 and 3 in the nucleus.
Study provide further evidence that pathogenic variants in Human immunodeficiency virus type I enhancer binding protein 2 lead to intellectual disabilities and developmental delay.
HIVEP2 loss-of-function mutations were identified in intellectual disability patients.
a 154-amino acid region of MIBP1 was necessary for its O-GlcNAc transferase binding and O-GlcNAcylation.
This gene encodes a member of a family of closely related, large, zinc finger-containing transcription factors. The encoded protein regulates transcription by binding to regulatory regions of various cellular and viral genes that maybe involved in growth, development and metastasis. The protein contains the ZAS domain comprised of two widely separated regions of zinc finger motifs, a stretch of highly acidic amino acids and a serine/threonine-rich sequence.
human immunodeficiency virus type I enhancer binding protein 2
, schnurri 2
, immunodeficiency virus type I enhancer-binding protein 2 homolog
, transcription factor HIVEP2-like
, human immunodeficiency virus type I enhancer-binding protein 2 homolog
, myc intron-binding protein 1
, transcription factor HIVEP2
, DNA-binding protein AGIE-BP1
, angiotensinogen gene-inducible enhancer-binding protein 1
, c-myc intron binding protein 1
, human immunodeficiency virus type 1 enhancer-binding protein 2
, MHC binding protein-2
, MHC-binding protein 2
, human immunodeficiency virus type I enhancer-binding protein 2