Ignet

Gene Information

Gene symbol: HSPA5

Gene name: heat shock 70kDa protein 5 (glucose-regulated protein, 78kDa)

HGNC ID: 5238

Synonyms: BiP

Related Genes

#	Gene Symbol	Number of hits
1	ALB	1 hits
2	ANGPTL3	1 hits
3	APOL1	1 hits
4	ATF6	1 hits
5	ATP2A2	1 hits
6	CASP1	1 hits
7	CASP12	1 hits
8	CASP3	1 hits
9	CD2AP	1 hits
10	CDK5	1 hits
11	CEBPA	1 hits
12	DDIT3	1 hits
13	EBP	1 hits
14	EIF1	1 hits
15	EIF2S1	1 hits
16	FUS	1 hits
17	GTF2A1	1 hits
18	HSP90B1	1 hits
19	NOX4	1 hits
20	NPHS1	1 hits
21	SALL1	1 hits
22	SH3D19	1 hits
23	VSIG4	1 hits
24	XBP1	1 hits

Related Sentences

#	PMID	Sentence
1	35086056	Podocyte protection by Angptl3 knockout via inhibiting ROS/GRP78 pathway in LPS-induced acute kidney injury.
2	35086056	Podocyte protection by Angptl3 knockout via inhibiting ROS/GRP78 pathway in LPS-induced acute kidney injury.
3	35086056	Then, the changes in renal function, podocyte apoptosis, inflammatory factors (tumor necrosis factor-α, TNF-α; interleukin-6, IL-6; and interleukin-1β, IL-1β), reactive oxygen species (ROS), and endoplasmic reticulum (ER) stress were measured.
4	35086056	Then, the changes in renal function, podocyte apoptosis, inflammatory factors (tumor necrosis factor-α, TNF-α; interleukin-6, IL-6; and interleukin-1β, IL-1β), reactive oxygen species (ROS), and endoplasmic reticulum (ER) stress were measured.
5	35086056	Angptl3 knockout was associated with the (1) downregulation of Bax and upregulation of Bcl-2; (2) amelioration of the abnormal expression of nephrin, podocin, and CD2AP; (3) reduced ER stress; (4) reduced secretions of TNF-α, IL-6, and IL-1β; and (5) regulation of Bax expression via the ROS-related ER stress pathway.
6	35086056	Angptl3 knockout was associated with the (1) downregulation of Bax and upregulation of Bcl-2; (2) amelioration of the abnormal expression of nephrin, podocin, and CD2AP; (3) reduced ER stress; (4) reduced secretions of TNF-α, IL-6, and IL-1β; and (5) regulation of Bax expression via the ROS-related ER stress pathway.
7	35086056	Our findings revealed that Angptl3 knockout alleviated the apoptosis of podocytes by regulating the ROS/GRP78 signaling pathway.
8	35086056	Our findings revealed that Angptl3 knockout alleviated the apoptosis of podocytes by regulating the ROS/GRP78 signaling pathway.
9	34993544	ER stress biomarkers (GRP78, p-eIF2α or CHOP), intracellular ROS generation, integrin-β3 and cell adhesion and migration were studied in a treatment of experiment using TGF-β1 with and without the ER stress inhibitors: 4-phenylbutyric acid (4-PBA, a chemical chaperone), salubrinal (an eIF2α dephosphorylation inhibitor) and N-acetylcysteine (NAC, an antioxidant).
10	34993544	ER stress biomarkers (GRP78, p-eIF2α or CHOP), intracellular ROS generation, integrin-β3 and cell adhesion and migration were studied in a treatment of experiment using TGF-β1 with and without the ER stress inhibitors: 4-phenylbutyric acid (4-PBA, a chemical chaperone), salubrinal (an eIF2α dephosphorylation inhibitor) and N-acetylcysteine (NAC, an antioxidant).
11	34993544	ER stress biomarkers (GRP78, p-eIF2α or CHOP), intracellular ROS generation, integrin-β3 and cell adhesion and migration were studied in a treatment of experiment using TGF-β1 with and without the ER stress inhibitors: 4-phenylbutyric acid (4-PBA, a chemical chaperone), salubrinal (an eIF2α dephosphorylation inhibitor) and N-acetylcysteine (NAC, an antioxidant).
12	34993544	ER stress biomarkers (p-eIF2α/eIF2α and GRP78), ROS generation and intergrin-β3 expression increased after TGF-β1 treatment.
13	34993544	ER stress biomarkers (p-eIF2α/eIF2α and GRP78), ROS generation and intergrin-β3 expression increased after TGF-β1 treatment.
14	34993544	ER stress biomarkers (p-eIF2α/eIF2α and GRP78), ROS generation and intergrin-β3 expression increased after TGF-β1 treatment.
15	34993544	NAC down-regulated the expression of GRP78 after TGF-β1 treatment. 4-PBA attenuated TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation and intergrin-β3 expression.
16	34993544	NAC down-regulated the expression of GRP78 after TGF-β1 treatment. 4-PBA attenuated TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation and intergrin-β3 expression.
17	34993544	NAC down-regulated the expression of GRP78 after TGF-β1 treatment. 4-PBA attenuated TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation and intergrin-β3 expression.
18	34993544	However, salubrinal did not inhibit TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation or integrin-β3 expression.
19	34993544	However, salubrinal did not inhibit TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation or integrin-β3 expression.
20	34993544	However, salubrinal did not inhibit TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation or integrin-β3 expression.
21	34993544	This study demonstrated that TGF-β1-induced ER stress potentiates the generation of intracellular ROS to a high degree through the PERK/eIF2α/CHOP pathway.
22	34993544	This study demonstrated that TGF-β1-induced ER stress potentiates the generation of intracellular ROS to a high degree through the PERK/eIF2α/CHOP pathway.
23	34993544	This study demonstrated that TGF-β1-induced ER stress potentiates the generation of intracellular ROS to a high degree through the PERK/eIF2α/CHOP pathway.
24	33323915	RESULTS Paclitaxel restored downregulated expression of nephrin and synaptopodin and upregulated VEGF expression after injury induced by palmitate.
25	33323915	Four endoplasmic reticulum stress markers, ATF-6alpha, Bip, CHOP, and spliced xBP1, were significantly increased in palmitate-treated podocytes compared with control podocytes.
26	33323915	Paclitaxel alleviated the expression levels of the antioxidant molecules, Nrf-2, HO-1, SOD-1, and SOD-2.
27	33323915	The paclitaxel effects were accompanied by inhibition of the inflammatory cytokines, MCP-1, TNF-alpha, TNF-R2, and TLR4, as well as attenuation of the apoptosis markers, Bax, Bcl-2, and Caspase-3.
28	31498850	CCL2/CCR2 signaling is believed to play an important role in kidney diseases.
29	31498850	We investigated the therapeutic effects and the mechanism of CCL2/CCR2 signaling in obesity-induced kidney injury.
30	31498850	HFD-induced elevated expressions of xBP1, Bip, and Nox4 at RNA and protein levels were significantly decreased in HFD KO.
31	31498850	Therefore, blockade of CCL2/CCR2 signaling by CCR2 depletion might ameliorate obesity-induced albuminuria through blocking oxidative stress, ER stress, and lipid accumulation.
32	29967295	Consistently, the expression levels of nephrin and podocin proteins were significantly decreased in the G1- or G2-overexpressing cells despite the maintenance of their mRNA expressions levels.
33	29967295	In contrast, the expression of the 78-kDa glucose-regulated protein ((GRP78), also known as the binding Ig protein, BiP) and the phosphorylation of the eukaryotic translation initiation factor 1 (eIF1) were significantly elevated in the G1/HPs and G2/HPs, suggesting a possible occurrence of ER stress in these cells.
34	29967295	Furthermore, ER stress inhibitors not only restored nephrin protein expression, but also provided protection against necrosis in G1/HPs and G2/HPs, suggesting that APOL1 risk variants cause podocyte injury partly through enhancing ER stress.
35	29843457	TAU limited proteinuria and podocytes foot processes effacement, and balanced slit diaphragm nephrin and glomerular claudin 1 expressions.
36	29843457	Remarkably, TAU downregulated glomerular ER stress markers (GRP78, GRP94), pro-apoptotic C/EBP homologous protein, activated caspase 3, tubular caspase1, and mitochondrial chaperone GRP75, but maintained anti-apoptotic HSP25.
37	28759006	To explore the significance of Sall1 in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1 KO^p°^d°^/p°^d°) using a podocin-Cre/loxP system and siRNA Sall1 knockdown (Sall1 KD) podocytes.
38	28759006	To explore the significance of Sall1 in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1 KO^p°^d°^/p°^d°) using a podocin-Cre/loxP system and siRNA Sall1 knockdown (Sall1 KD) podocytes.
39	28759006	To explore the significance of Sall1 in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1 KO^p°^d°^/p°^d°) using a podocin-Cre/loxP system and siRNA Sall1 knockdown (Sall1 KD) podocytes.
40	28759006	Differentiated Sall1 KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration.
41	28759006	Differentiated Sall1 KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration.
42	28759006	Differentiated Sall1 KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration.
43	28759006	These results indicated that Sall1 has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78.
44	28759006	These results indicated that Sall1 has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78.
45	28759006	These results indicated that Sall1 has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78.
46	28759006	GRP78 expression was higher in ADR-treated Sall1 KO^p°^d°^/p°^d° mice than in control mice.
47	28759006	GRP78 expression was higher in ADR-treated Sall1 KO^p°^d°^/p°^d° mice than in control mice.
48	28759006	GRP78 expression was higher in ADR-treated Sall1 KO^p°^d°^/p°^d° mice than in control mice.
49	28759006	Sall1 appeared to influence the expression of GRP78 in injured podocytes.
50	28759006	Sall1 appeared to influence the expression of GRP78 in injured podocytes.
51	28759006	Sall1 appeared to influence the expression of GRP78 in injured podocytes.
52	28385815	The enhanced expression of GRP78 by podocytes expressing APOL1 variants would indicate endoplasmic reticulum (ER) stress.
53	28066247	In palmitate stimulated podocytes, AS-IV markedly improved inhibitions of SERCA activity and SERCA2 expression, restored intracellular Ca²⁺ homeostasis, and attenuated podocyte apoptosis in a dose-dependent manner with a concomitant abrogation of ER stress as evidenced by the downregulation of GRP78, cleaved ATF6, phospho-IRE1α and phospho-PERK, and the inactivation of both ER stress-mediated and mitochondria-mediated apoptotic pathways.
54	28024901	Cyclin-dependent kinase 5 contributes to endoplasmic reticulum stress induced podocyte apoptosis via promoting MEKK1 phosphorylation at Ser280 in diabetic nephropathy.
55	28024901	Cyclin-dependent kinase 5 contributes to endoplasmic reticulum stress induced podocyte apoptosis via promoting MEKK1 phosphorylation at Ser280 in diabetic nephropathy.
56	28024901	The results showed that along with induction of Cdk5 and apoptosis, GRP78 and its two sensors as well as CHOP and cleaved caspase-12 were induced in high glucose treated podocytes.
57	28024901	The results showed that along with induction of Cdk5 and apoptosis, GRP78 and its two sensors as well as CHOP and cleaved caspase-12 were induced in high glucose treated podocytes.
58	28024901	The ER stress inducer, tunicamycin, also up-regulated the kinase activity and protein expression of Cdk5 in podocytes accompanied with the increasing of GRP78.
59	28024901	The ER stress inducer, tunicamycin, also up-regulated the kinase activity and protein expression of Cdk5 in podocytes accompanied with the increasing of GRP78.
60	28024901	On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation.
61	28024901	On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation.
62	28024901	Therefore, our study proved that Cdk5 may play an important role in ER stress induced podocyte apoptosis through MEKK1/JNK pathway in diabetic nephropathy.
63	28024901	Therefore, our study proved that Cdk5 may play an important role in ER stress induced podocyte apoptosis through MEKK1/JNK pathway in diabetic nephropathy.
64	27236787	Furthermore, animals with genetic ablation of UPR-activated transcription factor C/EBP homologous protein CHOP allocated in high-AGEs diet, exhibited relative resistance to UPR induction (BiP levels) and XBP1 activation in major metabolic organs.
65	26999661	These beneficial effects of UDCA or 4-PBA on DN were associated with the inhibition of ER stress, as evidenced by the decreased expression of BiP, phospho-IRE1α, phospho-eIF2α, CHOP, ATF-6 and spliced X-box binding protein-1 in vitro and in vivo.
66	26999661	UDCA or 4-PBA prevented hyperglycemia-induced or high glucose (HG)-induced apoptosis in podocytes in vivo and in vitro via the inhibition of caspase-3 and caspase-12 activation.
67	25322957	Thapsigargin/tunicamycin treatment induced a significant increase in endoplasmic reticulum stress and of cell death, represented by higher GADD153 and GRP78 expression and propidium iodide flow cytometry, respectively.
68	25173645	Renal remodeling, function, ER stress (CHOP and GRP78) and inflammation (infiltration of inflammatory cells, NF-κB p65) were evaluated 12 weeks after MI.
69	25173645	Renal remodeling, function, ER stress (CHOP and GRP78) and inflammation (infiltration of inflammatory cells, NF-κB p65) were evaluated 12 weeks after MI.
70	25173645	However, MI significantly increased the glomerular expression of GRP78 and CHOP in UNX and DB rats.
71	25173645	However, MI significantly increased the glomerular expression of GRP78 and CHOP in UNX and DB rats.
72	25173645	In addition, it also promoted the infiltration of CD4+ T cells, particularly inflammatory cytokine (IFN-γ, IL-17, IL-4)-producing CD4+ T cells, and the expression of NF-κB p65 in the glomeruli.
73	25173645	In addition, it also promoted the infiltration of CD4+ T cells, particularly inflammatory cytokine (IFN-γ, IL-17, IL-4)-producing CD4+ T cells, and the expression of NF-κB p65 in the glomeruli.
74	24503896	Glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP/GADD153) and caspase-12 expression was analyzed by RT-PCR, western blot analysis and immunocytochemistry.
75	24503896	CHOP/GADD153 expression reached its peak at 48 h, and caspase-12 expression gradually increased with time.
76	24503896	Spearman's correlation analysis revealed that caspase-12 and CHOP/GADD153 positively correlated with the apoptotic rate (r=0.915, P<0.01 and r=0.639, P<0.01).
77	21679752	Regulation of CD2-associated protein influences podocyte endoplasmic reticulum stress-mediated apoptosis induced by albumin overload.
78	21679752	Regulation of CD2-associated protein influences podocyte endoplasmic reticulum stress-mediated apoptosis induced by albumin overload.
79	21679752	Regulation of CD2-associated protein influences podocyte endoplasmic reticulum stress-mediated apoptosis induced by albumin overload.
80	21679752	In the present study, we investigated the role of CD2-associated protein (CD2AP) in protein overload-induced ER stress and subsequent podocyte apoptosis.
81	21679752	In the present study, we investigated the role of CD2-associated protein (CD2AP) in protein overload-induced ER stress and subsequent podocyte apoptosis.
82	21679752	In the present study, we investigated the role of CD2-associated protein (CD2AP) in protein overload-induced ER stress and subsequent podocyte apoptosis.
83	21679752	The expressions of GRP78, caspase-12 and CD2AP were detected by RT-PCR or Western blot analysis.
84	21679752	The expressions of GRP78, caspase-12 and CD2AP were detected by RT-PCR or Western blot analysis.
85	21679752	The expressions of GRP78, caspase-12 and CD2AP were detected by RT-PCR or Western blot analysis.
86	21679752	Accumulation of albumin in podocytes induced ER stress and apoptosis in a concentration-dependent manner as indicated by upregulation of GRP78 and caspase-12.
87	21679752	Accumulation of albumin in podocytes induced ER stress and apoptosis in a concentration-dependent manner as indicated by upregulation of GRP78 and caspase-12.
88	21679752	Accumulation of albumin in podocytes induced ER stress and apoptosis in a concentration-dependent manner as indicated by upregulation of GRP78 and caspase-12.
89	21679752	Transfection of CD2AP eukaryotic expression vector into podocytes increased CD2AP expression, depressed GRP78 and caspase-12 expressions, and inhibited podocyte apoptosis.
90	21679752	Transfection of CD2AP eukaryotic expression vector into podocytes increased CD2AP expression, depressed GRP78 and caspase-12 expressions, and inhibited podocyte apoptosis.
91	21679752	Transfection of CD2AP eukaryotic expression vector into podocytes increased CD2AP expression, depressed GRP78 and caspase-12 expressions, and inhibited podocyte apoptosis.
92	21679752	It is concluded protein overload induces podocyte apoptosis via ER stress and CD2AP may play a crucial role in albumin overload-induced ER stress and apoptosis in podocytes.
93	21679752	It is concluded protein overload induces podocyte apoptosis via ER stress and CD2AP may play a crucial role in albumin overload-induced ER stress and apoptosis in podocytes.
94	21679752	It is concluded protein overload induces podocyte apoptosis via ER stress and CD2AP may play a crucial role in albumin overload-induced ER stress and apoptosis in podocytes.
95	17687078	Induction of nephrotic-range proteinuria with puromycin aminonucleoside in mice increased expression of the ER stress marker GRP78 in podocytes, and led to the mislocalization of nephrin to the cytoplasm.