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抗人 GADD45B 抗体对
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抗人 GADD45B 抗体对

01AB02974

Growth arrest and DNA damage inducible beta (GADD45B) is a nuclear stress-response protein that plays a pivotal role in regulating cellular responses to environmental stress, growth arrest, and DNA damage. As a member of the GADD45 family, it functions by binding to upstream mitogen-activated protein kinase kinase kinases, such as MTK1/MEKK4, to modulate the p38 and JNK MAPK signaling pathways. This interaction influences critical cellular processes, including cell-cycle arrest, survival, and apoptosis. In the central nervous system, GADD45B acts as an epigenetic regulator by facilitating active DNA demethylation through base-excision repair mechanisms at specific gene promoters, such as BDNF and FGF. This activity is essential for neurogenesis, synaptic plasticity, and activity-dependent gene expression. Dysregulation of GADD45B is associated with various neuropsychiatric and neurological conditions, including autism spectrum disorders, schizophrenia, and epilepsy, as well as neurodegenerative processes in Parkinson’s disease models.

Human
规格起售价
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技术参数

靶点基因名
GADD45B
基因别名
MYD118
蛋白别名
growth arrest and DNA damage inducible beta; GADD45B
UniProt
O75293
物种
Human

产品详情

靶点名称
GADD45B
蛋白名称
growth arrest and DNA damage inducible beta
蛋白别名
Growth arrest and DNA damage-inducible protein GADD45 beta; Myeloid differentiation primary response protein MyD118; Negative growth regulatory protein MyD118
靶点基因名
GADD45B
基因别名
MYD118
UniProt
O75293
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Growth arrest and DNA damage inducible beta (GADD45B) is a nuclear stress-response protein that plays a pivotal role in regulating cellular responses to environmental stress, growth arrest, and DNA damage. As a member of the GADD45 family, it functions by binding to upstream mitogen-activated protein kinase kinase kinases, such as MTK1/MEKK4, to modulate the p38 and JNK MAPK signaling pathways. This interaction influences critical cellular processes, including cell-cycle arrest, survival, and apoptosis. In the central nervous system, GADD45B acts as an epigenetic regulator by facilitating active DNA demethylation through base-excision repair mechanisms at specific gene promoters, such as BDNF and FGF. This activity is essential for neurogenesis, synaptic plasticity, and activity-dependent gene expression. Dysregulation of GADD45B is associated with various neuropsychiatric and neurological conditions, including autism spectrum disorders, schizophrenia, and epilepsy, as well as neurodegenerative processes in Parkinson’s disease models.