(Q24306803)

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JAK/STAT3 pathway is involved in survival of neurons in response to insulin-like growth factor and negatively regulated by suppressor of cytokine signaling-3

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JAK/STAT3 pathway is involved in survival of neurons in response to insulin-like growth factor and negatively regulated by suppressor of cytokine signaling-3 (English)

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1 reference

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author name string

Ajay Yadav

1

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Anjana Kalita

2

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Shivani Dhillon

3

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Kakoli Banerjee

4

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language of work or name

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publication date

9 September 2005

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Journal of Biological Chemistry

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280

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36

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31830-40

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"Inflammatory" cytokines: neuromodulators in normal brain?

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Insulin-like growth factor-1 and post-ischemic brain injury

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RETRACTED: A new mechanism of neurodegeneration: a proinflammatory cytokine inhibits receptor signaling by a survival peptide

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Traumatic brain injury-induced acute gene expression changes in rat cerebral cortex identified by GeneChip analysis

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Inducers of oxidative stress block ciliary neurotrophic factor activation of Jak/STAT signaling in neurons.

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STAT signalling in the mature and aging brain.

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Negative regulation of the JAK/STAT pathway

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Cytokine signaling in the brain: putting a SOCS in it?

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SOCS-1 and SOCS-3 block insulin signaling by ubiquitin-mediated degradation of IRS1 and IRS2

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SOCS-3 inhibits insulin signaling and is up-regulated in response to tumor necrosis factor-alpha in the adipose tissue of obese mice

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Interaction of human suppressor of cytokine signaling (SOCS)-2 with the insulin-like growth factor-I receptor

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Cellular mechanisms associated with spontaneous and ciliary neurotrophic factor-cAMP-induced survival and axonal regeneration of adult retinal ganglion cells

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SOCS-3 is an insulin-induced negative regulator of insulin signaling

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Suppressor of cytokine signaling-3 preferentially binds to the SHP-2-binding site on the shared cytokine receptor subunit gp130

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Rescue of TNFalpha-inhibited neuronal cells by IGF-1 involves Akt and c-Jun N-terminal kinases

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Stats: transcriptional control and biological impact

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Functional subdomains of STAT2 required for preassociation with the alpha interferon receptor and for signaling

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An alternative pathway for STAT activation that is mediated by the direct interaction between JAK and STAT.

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Antiapoptotic effects of leptin in human neuroblastoma cells

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STATs: signal transducers and activators of transcription

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STATs and gene regulation

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Activation of STAT signaling pathways and induction of suppressors of cytokine signaling (SOCS) proteins in mammalian lens by growth factors

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SOCS2 induces neurite outgrowth by regulation of epidermal growth factor receptor activation

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Independent roles of SOCS-3 and SHP-2 in the regulation of neuronal gene expression by leukemia inhibitory factor.

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Socs3 deficiency in the brain elevates leptin sensitivity and confers resistance to diet-induced obesity

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Feedback inhibition of leptin receptor/Jak2 signaling via Tyr1138 of the leptin receptor and suppressor of cytokine signaling 3.

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Tumour necrosis factor alpha (TNF)-TNF receptor 1-inducible cytoprotective proteins in the mouse liver: relevance of suppressors of cytokine signalling.

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Gene expression changes after focal stroke, traumatic brain and spinal cord injuries

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Expression of TNF and TNF receptors (p55 and p75) in the rat brain after focal cerebral ischemia

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Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis

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The movement of IGF-I into the brain parenchyma after hypoxic-ischaemic injury.

1 reference

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7 January 2021

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Ciliary neurotrophic factor and stress stimuli activate the Jak-STAT pathway in retinal neurons and glia

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Different signaling pathways mediate regenerative versus developmental sensory axon growth.

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Identifiers

10.1074/JBC.M501316200

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

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